title: Notes on the hydrology of the Waikato River

authors: Ridall, G.T.

subjects: Waikato river

abstract: The catchment area of the Waikato River is 5,500 square miles. If its source is accepted as being the Upper Waikato, then its distance to the sea at Port Waikato including its journey through Lake Taupo is 266 miles. It rises, together with the Whangaehu, the Rangitikei and the Wanganui, between the volcanic region of Ruapehu 9,000 ft. above sea level and the Kaimanawa Ranges 5,000 ft. above sea level.
The river flows northwards for 34 miles into Lake Taupo, losing its identity into the Tongariro for the last 26 miles to the lake. It emerges from Lake Taupo resuming its proper name and, still flowing northwards, passes for more than 100 miles through a series of lakes formed by hydroelectric dams to Cambridge. From here it continues through a deeply incised channel to Ngaruawahia where it is joined by its major tributary, the Waipa River. From Ngaruawahia to the mouth, a distance of 60 miles, shallow lakes and peat swamps predominate on both sides of the river, many of them protected and drained and developed into rich dairy farms. From Mercer, 35 miles downstream of Ngaruawahia, where slight tidal effects are discernable at low flows, the river changes its general northerly direction to a westerly one and, still 9 miles from the mouth, enters the delta. Here it is fragmented into many channels before emptying into the broad expanse of Maioro Bay and finally emerges by two fairly narrow channels into the sea on the west coast, 25 miles south of Manukau Heads.

text: Notes on the hydrology of the Waikato River The catchment area of the Waikato River is 5,500 square miles. If its source is accepted as being the Upper Waikato, then its distance to the sea at Port Waikato including its journey through Lake Taupo is 266 miles. It rises, together with the Whangaehu, the Rangitikei and the Wanganui, between the volcanic region of Ruapehu 9,000 ft. above sea level and the Kaimanawa Ranges 5,000 ft. above sea level.
The river flows northwards for 34 miles into Lake Taupo, losing its identity into the Tongariro for the last 26 miles to the lake. It emerges from Lake Taupo resuming its proper name and, still flowing northwards, passes for more than 100 miles through a series of lakes formed by hydroelectric dams to Cambridge. From here it continues through a deeply incised channel to Ngaruawahia where it is joined by its major tributary, the Waipa River. From Ngaruawahia to the mouth, a distance of 60 miles, shallow lakes and peat swamps predominate on both sides of the river, many of them protected and drained and developed into rich dairy farms. From Mercer, 35 miles downstream of Ngaruawahia, where slight tidal effects are discernable at low flows, the river changes its general northerly direction to a westerly one and, still 9 miles from the mouth, enters the delta. Here it is fragmented into many channels before emptying into the broad expanse of Maioro Bay and finally emerges by two fairly narrow channels into the sea on the west coast, 25 miles south of Manukau Heads.

year: 1967

title: The role of intratidal oscillations in sediment resuspension in a diurnal, partially mixed estuary

authors: O’Callaghan, J.M.

subjects: diurnal tides

abstract: Using detailed observations of the mean and turbulent properties of flow, salinity and turbidity that spanned 2001/02, we examined the physical mechanisms underpinning sediment resuspension in the low-energy Swan River estuary, Western Australia. In this diurnal tidally-dominated estuary, the presence of intratidal oscillations, a tidal inequality lasting 2 to 3 hours on the flood tide, generated by interactions of the four main diurnal and semidiurnal astronomical constituents, K₁, O₁, M₂, and S₂, played a major role in modifying vertical stratification and mixing. These intratidal oscillations are controlled by phase differences between the tropic and synodic months rather than being temporally-fixed by bed friction, as occurs in semidiurnal estuaries. Intratidal oscillations are largest, at around 0.1 m, near to the Austral solstice when the lunar and solar declination are in-phase. Despite the seemingly small change in water level, shear-induced interfacial mixing caused destratification of the water column with the top-to-bottom salinity (ΔS) difference of 3.5 present early in the flood tide eroded to less than 0.3 by the end of the intratidal oscillation. High turbidity peaks, of 250 nephelometric turbidity units, coincided with these intratidal oscillations and could not be explained by bed friction since shear stress from mean flow did not exceed threshold criteria. High Reynolds stresses of ∼1 Nm⁻² did, however, exceed τcr and together with negative Reynolds fluxes indicate a net downward transport of material. Destratification of the water column induced by shear instabilities resulted in large overturns capable of moving in situ material towards the bed during intratidal oscillations and these turbidities were ∼10 times greater than those from bed-generated resuspension observed later during the flood tide.

text: The role of intratidal oscillations in sediment resuspension in a diurnal, partially mixed estuary Using detailed observations of the mean and turbulent properties of flow, salinity and turbidity that spanned 2001/02, we examined the physical mechanisms underpinning sediment resuspension in the low-energy Swan River estuary, Western Australia. In this diurnal tidally-dominated estuary, the presence of intratidal oscillations, a tidal inequality lasting 2 to 3 hours on the flood tide, generated by interactions of the four main diurnal and semidiurnal astronomical constituents, K₁, O₁, M₂, and S₂, played a major role in modifying vertical stratification and mixing. These intratidal oscillations are controlled by phase differences between the tropic and synodic months rather than being temporally-fixed by bed friction, as occurs in semidiurnal estuaries. Intratidal oscillations are largest, at around 0.1 m, near to the Austral solstice when the lunar and solar declination are in-phase. Despite the seemingly small change in water level, shear-induced interfacial mixing caused destratification of the water column with the top-to-bottom salinity (ΔS) difference of 3.5 present early in the flood tide eroded to less than 0.3 by the end of the intratidal oscillation. High turbidity peaks, of 250 nephelometric turbidity units, coincided with these intratidal oscillations and could not be explained by bed friction since shear stress from mean flow did not exceed threshold criteria. High Reynolds stresses of ∼1 Nm⁻² did, however, exceed τcr and together with negative Reynolds fluxes indicate a net downward transport of material. Destratification of the water column induced by shear instabilities resulted in large overturns capable of moving in situ material towards the bed during intratidal oscillations and these turbidities were ∼10 times greater than those from bed-generated resuspension observed later during the flood tide.

year: 2010

title: Epidemiological evidence that can help to improve timely diagnosis of colorectal cancer in New Zealand.

authors: Hirsz, Malgorzata

subjects: Colorectal cancer

abstract: Incidence rates of colorectal cancer (CRC) in New Zealand (NZ) are among the highest in the world. The long-term survival rates in NZ are poor, which has partially been attributed to late diagnosis. Considering that CRC is a curable disease if diagnosed early, conducting research targeted at the improvement of early diagnosis is therefore important. This thesis provides statistical models for the calculation of CRC incidence rates in the entire NZ population and population strata defined by age, gender, ethnicity and diabetes status, and a model for CRC risk in individual patients referred to the secondary care. The models presented here could assist health professionals in the selection of patients for further investigation to facilitate earlier diagnosis. The empirical part consists of three independent observational studies, briefly described below.

Sub-study 1. The objectives were, first, to describe trends in CRC incidence in the NZ population and, second, to investigate whether there are any strata defined by gender and ethnicity with especially increased incidence rates of CRC. To address these objectives, I analysed data from the New Zealand Cancer Registry (years 1994–2018) using an age- period-cohort (APC) model. The overall CRC incidence rates in NZ decreased between 1994 and 2018 by an average of 1.31% per year. However, the decrease was observed only in patients 50 years and older. In those 30-<50 years old, the incidence rates increased between 1994 and 2018 regardless of gender and ethnicity. The increase was similar for proximal, distal and rectal cancers. The APC analyses revealed very strong cohort effects that could explain nearly the entire trends in CRC incidence, pointing out generations born in the 1970s and 80s being affected by the increased incidence rates, rather than individuals 30-<50 years old. The cohort effects were different in Ma ̄ori and non-Ma ̄ori populations. In non-Ma ̄ori born between approximately 1939 and 1955, incidence rates decreased sharply. By contrast, those Ma ̄ori generations have not benefitted from the sharp decrease in rates. However, CRC incidence increased substantially in both M ̄aori and non-M ̄aori groups born in the 1970s and 80s.

Sub-study 2. The objective was to estimate the IRR for CRC in patients with diabetes compared to those without diabetes, with relation to diabetes duration and use of insulin for diabetes control. Registration in the Virtual Diabetes Register (VDR) in the years 2014–2018 was used as a marker of a diabetes diagnosis. Tables with counts of the entire NZ population stratified by age, gender, and ethnicity were obtained from Statistics NZ. In total, data from 310,710 patients with diabetes, corresponding to 1,277,284 person- years and 2512 incident CRC cases were analysed using a Poisson regression model. Diabetes was associated with an overall increased CRC incidence of 13% compared to non-diabetes [IRR=1.13 (95% CI: 1.08, 1.18)]. The IRR was especially high in the first three months after diabetes diagnosis [IRR=2.55 (95% CI 2.02, 3.21)], likely due to detection bias. The association was equally strong in males and females. However, in the analysis by ethnicity, the incidence of CRC was increased only in non-Ma ̄ori patients and restricted only to those younger than 75 years.

Sub-study 3. The objective was to develop a predictive model for CRC risk in individual patients referred to secondary care. To develop such a model, I extracted information from free text included in e-referrals from GPs’ to the Gastroenterology and General Surgery departments in the Waikato Hospital from 2015-2018, including: symptoms; test results; and family history of CRC. The reference test was a full colonoscopy with visualisation of the cecum. Data from 3015 patients, 20-<90 years old were analysed using a logistic regression model. The final model included the following predictors associated with increased CRC risk: anaemia, rectal bleeding, palpable mass in abdomen or rectum, weight loss, age and gender, and a decreased CRC risk: family history of CRC, abdominal pain, and inflammatory bowel disease. The model discriminates patients with low CRC risk well. According to the final cross-validated model, around 20% of patients from our cohort had performed colonoscopy despite a very low CRC risk (less than 1.5%).

In conclusion, the APC analysis revealed an alarming pattern. According to the fitted APC model, the combination of increasing age and cohort effect in generations born in the 1970s and 80s will bring a wave of CRC diagnoses in the near future when the young generations with high CRC incidence rates will replace the old generations with low CRC incidence. The results from this study could therefore help policy-makers to plan the needs for gastroenterology services.
Secondly, CRC incidence rates in diabetes have been found to be slightly increased com- pared to non-diabetes but only in non-Ma ̄ori individuals younger than 75 years.
Third, the results suggest that males underutilise health services. As shown in sub- study 3, males underwent fewer colonoscopies than females, despite having a higher risk of CRC. The higher detection bias in males than in females (sub-study 2) could also suggest underuse of health services by males, but the difference was not statistically significant.
Finally, based on the fitted models for CRC incidence in sub-studies 1 and 2, population- wide CRC screening for Ma ̄ori and patients with diabetes, based on the incidence, instead of age alone, would be proposed to start at age 57.5 years if the screening in the general population starts at age 60 years.

text: Epidemiological evidence that can help to improve timely diagnosis of colorectal cancer in New Zealand. Incidence rates of colorectal cancer (CRC) in New Zealand (NZ) are among the highest in the world. The long-term survival rates in NZ are poor, which has partially been attributed to late diagnosis. Considering that CRC is a curable disease if diagnosed early, conducting research targeted at the improvement of early diagnosis is therefore important. This thesis provides statistical models for the calculation of CRC incidence rates in the entire NZ population and population strata defined by age, gender, ethnicity and diabetes status, and a model for CRC risk in individual patients referred to the secondary care. The models presented here could assist health professionals in the selection of patients for further investigation to facilitate earlier diagnosis. The empirical part consists of three independent observational studies, briefly described below.

Sub-study 1. The objectives were, first, to describe trends in CRC incidence in the NZ population and, second, to investigate whether there are any strata defined by gender and ethnicity with especially increased incidence rates of CRC. To address these objectives, I analysed data from the New Zealand Cancer Registry (years 1994–2018) using an age- period-cohort (APC) model. The overall CRC incidence rates in NZ decreased between 1994 and 2018 by an average of 1.31% per year. However, the decrease was observed only in patients 50 years and older. In those 30-<50 years old, the incidence rates increased between 1994 and 2018 regardless of gender and ethnicity. The increase was similar for proximal, distal and rectal cancers. The APC analyses revealed very strong cohort effects that could explain nearly the entire trends in CRC incidence, pointing out generations born in the 1970s and 80s being affected by the increased incidence rates, rather than individuals 30-<50 years old. The cohort effects were different in Ma ̄ori and non-Ma ̄ori populations. In non-Ma ̄ori born between approximately 1939 and 1955, incidence rates decreased sharply. By contrast, those Ma ̄ori generations have not benefitted from the sharp decrease in rates. However, CRC incidence increased substantially in both M ̄aori and non-M ̄aori groups born in the 1970s and 80s.

Sub-study 2. The objective was to estimate the IRR for CRC in patients with diabetes compared to those without diabetes, with relation to diabetes duration and use of insulin for diabetes control. Registration in the Virtual Diabetes Register (VDR) in the years 2014–2018 was used as a marker of a diabetes diagnosis. Tables with counts of the entire NZ population stratified by age, gender, and ethnicity were obtained from Statistics NZ. In total, data from 310,710 patients with diabetes, corresponding to 1,277,284 person- years and 2512 incident CRC cases were analysed using a Poisson regression model. Diabetes was associated with an overall increased CRC incidence of 13% compared to non-diabetes [IRR=1.13 (95% CI: 1.08, 1.18)]. The IRR was especially high in the first three months after diabetes diagnosis [IRR=2.55 (95% CI 2.02, 3.21)], likely due to detection bias. The association was equally strong in males and females. However, in the analysis by ethnicity, the incidence of CRC was increased only in non-Ma ̄ori patients and restricted only to those younger than 75 years.

Sub-study 3. The objective was to develop a predictive model for CRC risk in individual patients referred to secondary care. To develop such a model, I extracted information from free text included in e-referrals from GPs’ to the Gastroenterology and General Surgery departments in the Waikato Hospital from 2015-2018, including: symptoms; test results; and family history of CRC. The reference test was a full colonoscopy with visualisation of the cecum. Data from 3015 patients, 20-<90 years old were analysed using a logistic regression model. The final model included the following predictors associated with increased CRC risk: anaemia, rectal bleeding, palpable mass in abdomen or rectum, weight loss, age and gender, and a decreased CRC risk: family history of CRC, abdominal pain, and inflammatory bowel disease. The model discriminates patients with low CRC risk well. According to the final cross-validated model, around 20% of patients from our cohort had performed colonoscopy despite a very low CRC risk (less than 1.5%).

In conclusion, the APC analysis revealed an alarming pattern. According to the fitted APC model, the combination of increasing age and cohort effect in generations born in the 1970s and 80s will bring a wave of CRC diagnoses in the near future when the young generations with high CRC incidence rates will replace the old generations with low CRC incidence. The results from this study could therefore help policy-makers to plan the needs for gastroenterology services.
Secondly, CRC incidence rates in diabetes have been found to be slightly increased com- pared to non-diabetes but only in non-Ma ̄ori individuals younger than 75 years.
Third, the results suggest that males underutilise health services. As shown in sub- study 3, males underwent fewer colonoscopies than females, despite having a higher risk of CRC. The higher detection bias in males than in females (sub-study 2) could also suggest underuse of health services by males, but the difference was not statistically significant.
Finally, based on the fitted models for CRC incidence in sub-studies 1 and 2, population- wide CRC screening for Ma ̄ori and patients with diabetes, based on the incidence, instead of age alone, would be proposed to start at age 57.5 years if the screening in the general population starts at age 60 years.

year: 2021