Crop Updates 2002 - Oilseeds

This session covers twenty seven papers from different authors: 1. Forward and acknowledgements, Dave Eksteen, ACTING MANAGER OILSEEDS PRODUCTIVITY AND INDUSTRY DEVELOPMENT Department of Agriculture PLENARY SESSION 2. GMO canola - Track record in Canada, K. Neil Harker and George W. Clayton,Agriculture and Agri-Food Canada, Lacombe Research Centre, Lacombe, Alberta, R. Keith Downey, Agriculture and Agri-Food Canada, Saskatoon Research Centre, Saskatoon, Saskatchewan 3. GMO canola – Prospects in Western Australia farming systems, Keith Alcock, Crop Improvement Institute, Department of Agriculture 4. Diamondback moth (DBM) in canola, Kevin Walden, Department of Agriculture CANOLA AGRONOMY 5. Getting the best out of canola in the low rainfall central wheatbelt, Bevan Addison and Peter Carlton, Elders Ltd 6. Canola variety performance in Western Australia, Kevin Morthorpe, Stephen Addenbrooke and Alex Ford, Pioneer Hi-Bred Australia P/L 7. Relative performance of new canola varieties in Department of Agriculture variety trials in 2000 and 2001, S. Hasan Zaheer, GSARI, Department of Agriculture, G. Walton, Crop Improvement Institute, Department of Agriculture 8. Which canola cultivar should I sow? Imma Farré, CSIRO Plant Industry, Floreat, Bill Bowden,Western Australia Department of Agriculture 9. The effect of seed generation and seed source on yield and quality of canola, Paul Carmody, Department of Agriculture 10. The accumulation of oil in Brassica species, J.A. Fortescue and D.W. Turner, Plant Biology, Faculty of Natural and Agricultural Sciences, The University of Western Australia, B. Tan, PO Box 1249, South Perth 11. Potential and performance of alternative oilseeds in WA, Margaret C. Campbell, Centre for Legumes in Mediterranean Agriculture 12. Comparison of oilseed crops in WA, Ian Pritchard and Paul Carmody, Department of Agriculture, Centre for Cropping Systems, Margaret Campbell, Centre for Legumes in Mediterranean Agriculture 13. Identifying constraints to canola production, Dave Eksteen, Canola Development Officer, Department of Agriculture 14. Boron – should we be worried about it? Richard W. BellA, K. FrostA, Mike WongB, and Ross BrennanC , ASchool of Environmental Science, Murdoch University, BCSIRO Land and Water, CDepartment of Agriculture PEST AND DISEASE 15. Yield losses caused when Beet Western Yellows Virus infects canola, Roger Jones and Jenny Hawkes, Department of Agriculture, and Centre for Legumes in Mediterranean Agriculture 16. Influence of climate on aphid outbreaks and virus epidemics in canola, Debbie Thackray, Jenny Hawkes and Roger Jones, Centre for Legumes in Mediterranean Agriculture and Department of Agriculture 17. The annual shower of blackleg ascospores in canola: Can we predict and avoid it? Moin U. Salam, Ravjit K. Khangura, Art J. Diggle and Martin J. Barbetti, Department of Agriculture 18. Environmental influences on production and release of ascospores of blackleg and their implications in blackleg management in canola, Ravjit K. Khangura, Martin J. Barbetti , Moin U. Salam and Art J. Diggle, Department of Agriculture 19. WA blackleg resistance ratings on canola varieties form 2002, Ravjit Khangura, Martin J. Barbetti and Graham Walton, Department of Agriculture 20. Bronzed field beetle management in canola, Phil Michael, Department of Agriculture 21. DBM control in canola: Aerial versus boom application, Paul Carmody, Department of Agriculture 22. Effect of single or multiple spray trearments on the control of Diamondback moth (Plutella xylostella) and yield of canola at Wongan Hills, Françoise Berlandier, Paul Carmody and Christiaan Valentine, Department of Agriculture ESTABLISHMENT 23. GrainGuardÔ - A biosecurity plan for the canola industry, Greg Shea, Department of Agriculture 24. Large canola seed is best, particularly for deep sowing, Glen Riethmuller, Rafiul Alam, Greg Hamilton and Jo Hawksley, Department of Agriculture 25. Canola establishment with seed size, tines and discs, with and without stubble, Glen Riethmuller, Rafiul Alam, Greg Hamilton and Jo Hawksley, Department of Agriculture WEEDS 26. Role of Roundup ReadyÒ canola in the farming system, Art Diggle1, Patrick Smith2, Paul Neve3, Felicity Flugge4, Amir Abadi5, Stephen Powles3 1Department of Agriculture, 2CSIRO, Sustainable Ecosystems, 3Western Australian Herbicide Resistance Initiative, University of Western Australia, 4Centre for Legumes in Mediterranean Agriculture, University of Western Australia, 5Touchstone Consulting, Mt Hawthorn FEED 27. Getting value from canola meals in the animal feed industries: Aquaculture, Brett Glencross and John Curnow, Department of Fisheries - Government of Western Australia and Wayne Hawkins, Department of Agricultur

Effects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort

\ua9 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseBackground: Individuals with rare kidney diseases account for 5–10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure. Methods: People aged 0–96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan–Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1\ub773 m2 or more to first eGFR of less than 30 mL/min per 1\ub773 m2 (the therapeutic trial window). Findings: Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9\ub76 years (IQR 5\ub79–16\ub77). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2\ub781 million UK patients with all-cause chronic kidney disease (28% vs 1%; p<0\ub70001), but better survival rates (standardised mortality ratio 0\ub742 [95% CI 0\ub732–0\ub752]; p<0\ub70001). Median age at kidney failure, median age at death, time from start of dialysis to death, time from diagnosis to eGFR thresholds, and therapeutic trial window all varied substantially between rare diseases. Interpretation: Patients with rare kidney diseases differ from the general population of individuals with chronic kidney disease: they have higher 5-year rates of kidney failure but higher survival than other patients with chronic kidney disease stages 3–5, and so are over-represented in the cohort of patients requiring kidney replacement therapy. Addressing unmet therapeutic need for patients with rare kidney diseases could have a large beneficial effect on long-term kidney replacement therapy demand. Funding: RaDaR is funded by the Medical Research Council, Kidney Research UK, Kidney Care UK, and the Polycystic Kidney Disease Charity

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Effects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort

Background Individuals with rare kidney diseases account for 5–10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure. Methods People aged 0–96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan–Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1·73 m2 or more to first eGFR of less than 30 mL/min per 1·73 m2 (the therapeutic trial window). Findings Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9·6 years (IQR 5·9–16·7). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2·81 million UK patients with all-cause chronic kidney disease (28% vs 1%; p<0·0001), but better survival rates (standardised mortality ratio 0·42 [95% CI 0·32–0·52]; p<0·0001). Median age at kidney failure, median age at death, time from start of dialysis to death, time from diagnosis to eGFR thresholds, and therapeutic trial window all varied substantially between rare diseases. Interpretation Patients with rare kidney diseases differ from the general population of individuals with chronic kidney disease: they have higher 5-year rates of kidney failure but higher survival than other patients with chronic kidney disease stages 3–5, and so are over-represented in the cohort of patients requiring kidney replacement therapy. Addressing unmet therapeutic need for patients with rare kidney diseases could have a large beneficial effect on long-term kidney replacement therapy demand. Funding RaDaR is funded by the Medical Research Council, Kidney Research UK, Kidney Care UK, and the Polycystic Kidney Disease Charity

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome

Thigh-length compression stockings and DVT after stroke

Controversy exists as to whether neoadjuvant chemotherapy improves survival in patients with invasive bladder cancer, despite randomised controlled trials of more than 3000 patients. We undertook a systematic review and meta-analysis to assess the effect of such treatment on survival in patients with this disease