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1. Inhospital death is a biased measure of fatal outcome from bloodstream infection

Author

Laupland KB, Pasquill K, Parfitt EC, Dagasso G, Gupta K, and Steele L

Subjects
Mortality, case-fatality, bacteremia, Infectious and parasitic diseases, RC109-216
Abstract

Kevin B Laupland,1 Kelsey Pasquill,2 Elizabeth C Parfitt,1 Gabrielle Dagasso,1 Kaveri Gupta,1 Lisa Steele2 1Department of Medicine, Royal Inland Hospital, Kamloops, BC, Canada; 2Department of Pathology and Laboratory Medicine, Royal Inland Hospital, Kamloops, BC, Canada Purpose: Inhospital death is commonly used as an outcome measure. However, it may be a biased measure of overall fatal outcome. The objective of this study was to evaluate inhospital death as a measure of all-cause 30-day case fatality in patients with bloodstream infection (BSI).Patients and methods: A population-based surveillance cohort study was conducted, and patients who died in hospital within 30 days (30-day inhospital death) were compared with those who died in any location by day 30 post BSI diagnosis (30-day all-cause case fatality).Results: A total of 1,773 residents had first incident episodes of BSI. Overall, 299 patients died for a 30-day all-cause case fatality rate of 16.9%. Most (1,587; 89.5%) of the patients were admitted to hospital, and ten (5.4%) of the 186 patients not admitted to hospital died. Of the 1,587 admitted patients, 242 died for a 30-day inhospital death rate of 15.2%. A further 47 patients admitted to hospital died after discharge but within 30 days of BSI diagnosis for a 30-day case fatality rate among admitted patients of 18.2%. Patients who died following discharge within 30 days were older and more likely to have dementia.Conclusion: The use of inhospital death is a biased measure of true case fatality. Keywords: mortality, case fatality, bacteremia

Published
2019

4. Assessing Aeolus Aerosol Observational Capabilities for Data Assimilation in Air Quality and NWP Models

Author

Proestakis, E., Benedetti, A., Dabas, A., Amiridis, V., Marinou, E., Paschou, P., Georgiou, A., Gkikas, A., Kampouri, A., Gialitaki, A., Tsekeri, A., McLean, W., Steele, L., Sullivan, John T., editor, Leblanc, Thierry, editor, Tucker, Sara, editor, Demoz, Belay, editor, Eloranta, Edwin, editor, Hostetler, Chris, editor, Ishii, Shoken, editor, Mona, Lucia, editor, Moshary, Fred, editor, Papayannis, Alexandros, editor, and Rupavatharam, Krishna, editor

Published
2023
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5. Boston biorepository, recruitment and integrative network (BBRAIN): A resource for the Gulf War Illness scientific community

Author

Keating, D, Zundel, CG, Abreu, M, Krengel, M, Aenlle, K, Nichols, MD, Toomey, R, Chao, LL, Golier, J, Abdullah, L, Quinn, E, Heeren, T, Groh, JR, Koo, BB, Killiany, R, Loggia, ML, Younger, J, Baraniuk, J, Janulewicz, P, Ajama, J, Quay, M, Baas, PW, Qiang, L, Conboy, L, Kokkotou, E, O'Callaghan, JP, Steele, L, Klimas, N, and Sullivan, K

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Pain Research, Chronic Pain, Clinical Research, Boston, Humans, Information Dissemination, Magnetic Resonance Imaging, Persian Gulf Syndrome, Positron-Emission Tomography, Saliva, BBRAIN, GWI, GWIC, Gulf war, Gulf war illness, Biochemistry and Cell Biology, Pharmacology and Pharmaceutical Sciences, Pharmacology & Pharmacy, Biochemistry and cell biology, Pharmacology and pharmaceutical sciences
Abstract

AimsGulf War Illness (GWI), a chronic debilitating disorder characterized by fatigue, joint pain, cognitive, gastrointestinal, respiratory, and skin problems, is currently diagnosed by self-reported symptoms. The Boston Biorepository, Recruitment, and Integrative Network (BBRAIN) is the collaborative effort of expert Gulf War Illness (GWI) researchers who are creating objective diagnostic and pathobiological markers and recommend common data elements for GWI research.Main methodsBBRAIN is recruiting 300 GWI cases and 200 GW veteran controls for the prospective study. Key data and biological samples from prior GWI studies are being merged and combined into retrospective datasets. They will be made available for data mining by the BBRAIN network and the GWI research community. Prospective questionnaire data include general health and chronic symptoms, demographics, measures of pain, fatigue, medical conditions, deployment and exposure histories. Available repository biospecimens include blood, plasma, serum, saliva, stool, urine, human induced pluripotent stem cells and cerebrospinal fluid.Key findingsTo date, multiple datasets have been merged and combined from 15 participating study sites. These data and samples have been collated and an online request form for repository requests as well as recommended common data elements have been created. Data and biospecimen sample requests are reviewed by the BBRAIN steering committee members for approval as they are received.SignificanceThe BBRAIN repository network serves as a much needed resource for GWI researchers to utilize for identification and validation of objective diagnostic and pathobiological markers of the illness.

Published
2021

6. Unexpected nascent atmospheric emissions of three ozone-depleting hydrochlorofluorocarbons

Author

Vollmer, Martin K, Mühle, Jens, Henne, Stephan, Young, Dickon, Rigby, Matthew, Mitrevski, Blagoj, Park, Sunyoung, Lunder, Chris R, Rhee, Tae Siek, Harth, Christina M, Hill, Matthias, Langenfelds, Ray L, Guillevic, Myriam, Schlauri, Paul M, Hermansen, Ove, Arduini, Jgor, Wang, Ray HJ, Salameh, Peter K, Maione, Michela, Krummel, Paul B, Reimann, Stefan, O’Doherty, Simon, Simmonds, Peter G, Fraser, Paul J, Prinn, Ronald G, Weiss, Ray F, and Steele, L Paul

Subjects
Montreal Protocol, atmospheric composition, ozone depletion
Abstract

Global and regional atmospheric measurements and modeling can play key roles in discovering and quantifying unexpected nascent emissions of environmentally important substances. We focus here on three hydrochlorofluorocarbons (HCFCs) that are restricted by the Montreal Protocol because of their roles in stratospheric ozone depletion. Based on measurements of archived air samples and on in situ measurements at stations of the Advanced Global Atmospheric Gases Experiment (AGAGE) network, we report global abundances, trends, and regional enhancements for HCFC-132b ([Formula: see text]), which is newly discovered in the atmosphere, and updated results for HCFC-133a ([Formula: see text]) and HCFC-31 ([Formula: see text]ClF). No purposeful end-use is known for any of these compounds. We find that HCFC-132b appeared in the atmosphere 20 y ago and that its global emissions increased to 1.1 Gg⋅y-1 by 2019. Regional top-down emission estimates for East Asia, based on high-frequency measurements for 2016-2019, account for ∼95% of the global HCFC-132b emissions and for ∼80% of the global HCFC-133a emissions of 2.3 Gg⋅y-1 during this period. Global emissions of HCFC-31 for the same period are 0.71 Gg⋅y-1 Small European emissions of HCFC-132b and HCFC-133a, found in southeastern France, ceased in early 2017 when a fluorocarbon production facility in that area closed. Although unreported emissive end-uses cannot be ruled out, all three compounds are most likely emitted as intermediate by-products in chemical production pathways. Identification of harmful emissions to the atmosphere at an early stage can guide the effective development of global and regional environmental policy.

Published
2021

8. Risk-reducing mastectomy and breast cancer mortality in women with a BRCA1 or BRCA2 pathogenic variant: an international analysis

Author

Metcalfe, K, Huzarski, T, Gronwald, J, Kotsopoulos, J, Kim, R, Moller, P, Pal, T, Aeilts, A, Eisen, A, Karlan, B, Bordeleau, L, Tung, N, Olopade, O, Zakalik, D, Singer, C, Foulkes, W, Couch, F, Neuhausen, S, Eng, C, Sun, P, Lubinski, J, Narod, S, Velsher, L, Poll, A, Warner, E, Mccuaig, J, Armel, S, Saal, H, Steele, L, Lemire, E, Serfas, K, Senter, L, Sweet, K, Panchal, S, Cullinane, C, Blum, J, Rayson, D, Ramon y Cajal, T, Dungan, J, Fruscio, R, Zovato, S, Cohen, S, Metcalfe K., Huzarski T., Gronwald J., Kotsopoulos J., Kim R., Moller P., Pal T., Aeilts A., Eisen A., Karlan B., Bordeleau L., Tung N., Olopade O., Zakalik D., Singer C. F., Foulkes W., Couch F., Neuhausen S. L., Eng C., Sun P., Lubinski J., Narod S. A., Velsher L., Poll A., Warner E., McCuaig J., Armel S., Saal H., Steele L., Lemire E., Serfas K., Senter L., Sweet K., Panchal S., Cullinane C. A., Blum J. L., Rayson D., Ramon y Cajal T., Dungan J., Fruscio R., Zovato S., Cohen S., Metcalfe, K, Huzarski, T, Gronwald, J, Kotsopoulos, J, Kim, R, Moller, P, Pal, T, Aeilts, A, Eisen, A, Karlan, B, Bordeleau, L, Tung, N, Olopade, O, Zakalik, D, Singer, C, Foulkes, W, Couch, F, Neuhausen, S, Eng, C, Sun, P, Lubinski, J, Narod, S, Velsher, L, Poll, A, Warner, E, Mccuaig, J, Armel, S, Saal, H, Steele, L, Lemire, E, Serfas, K, Senter, L, Sweet, K, Panchal, S, Cullinane, C, Blum, J, Rayson, D, Ramon y Cajal, T, Dungan, J, Fruscio, R, Zovato, S, Cohen, S, Metcalfe K., Huzarski T., Gronwald J., Kotsopoulos J., Kim R., Moller P., Pal T., Aeilts A., Eisen A., Karlan B., Bordeleau L., Tung N., Olopade O., Zakalik D., Singer C. F., Foulkes W., Couch F., Neuhausen S. L., Eng C., Sun P., Lubinski J., Narod S. A., Velsher L., Poll A., Warner E., McCuaig J., Armel S., Saal H., Steele L., Lemire E., Serfas K., Senter L., Sweet K., Panchal S., Cullinane C. A., Blum J. L., Rayson D., Ramon y Cajal T., Dungan J., Fruscio R., Zovato S., and Cohen S.

Abstract

Background: Risk-reducing mastectomy (RRM) is offered to women with a BRCA1 or BRCA2 pathogenic variant, however, there are limited data on the impact on breast cancer mortality. Methods: Participants were identified from a registry of women with BRCA1/2 pathogenic variants. We used a pseudo-randomised trial design and matched one woman with a RRM to one woman without a RRM on year of birth, gene, and country. We estimated the hazard ratio (HR) and 95% confidence intervals (CI) for dying of breast cancer in the follow-up period. Results: There were 1654 women included; 827 assigned to the RRM arm and 827 assigned to the control arm. After a mean follow-up of 6.3 years, there were 20 incident breast cancers (including 15 occult cancers) and two breast cancer deaths in the RRM arm, and 100 incident breast cancers and 7 breast cancer deaths in the control arm (HR = 0.26; 95% CI 0.05–1.35; p = 0.11). The probability of dying of breast cancer within 15 years after RRM was 0.95%. Conclusions: In women with a BRCA1 or BRCA2 pathogenic variant, RRM reduces the risk of breast cancer, and the probability of dying of breast cancer is low.

Published
2024

9. Perfluorocyclobutane (PFC-318, c-C4F8) in the global atmosphere

Author

Muhle, Jens, Trudinger, Cathy M, Western, Luke M, Rigby, Matthew, Vollmer, Martin K, Park, Sunyoung, Manning, Alistair J, Say, Daniel, Ganesan, Anita, Steele, L Paul, Ivy, Diane J, Arnold, Tim, Li, Shanlan, Stohl, Andreas, Harth, Christina M, Salameh, Peter K, McCulloch, Archie, O'Doherty, Simon, Park, Mi-Kyung, Jo, Chun Ok, Young, Dickon, Stanley, Kieran M, Krummel, Paul B, Mitrevski, Blagoj, Hermansen, Ove, Lunder, Chris, Evangeliou, Nikolaos, Yao, Bo, Kim, Jooil, Hmiel, Benjamin, Buizert, Christo, Petrenko, Vasilii V, Arduini, Jgor, Maione, Michela, Etheridge, David M, Michalopoulou, Eleni, Czerniak, Mike, Severinghaus, Jeffrey P, Reimann, Stefan, Simmonds, Peter G, Fraser, Paul J, Prinn, Ronald G, and Weiss, Ray F

Subjects
Astronomical and Space Sciences, Atmospheric Sciences, Meteorology & Atmospheric Sciences
Abstract

Abstract. We reconstruct atmospheric abundances of the potentgreenhouse gas c-C4F8 (perfluorocyclobutane, perfluorocarbonPFC-318) from measurements of in situ, archived, firn, and aircraft airsamples with precisions of ∼1 %–2 % reported on the SIO-14gravimetric calibration scale. Combined with inverse methods, we found near-zero atmospheric abundances from the early 1900s to the early 1960s, afterwhich they rose sharply, reaching 1.66 ppt (parts per trillion dry-air molefraction) in 2017. Global c-C4F8 emissions rose from near zero inthe 1960s to 1.2±0.1 (1σ) Gg yr−1 in the late 1970s tolate 1980s, then declined to 0.77±0.03 Gg yr−1 in the mid-1990sto early 2000s, followed by a rise since the early 2000s to 2.20±0.05 Gg yr−1 in 2017. These emissions are significantly larger thaninventory-based emission estimates. Estimated emissions from eastern Asiarose from 0.36 Gg yr−1 in 2010 to 0.73 Gg yr−1 in 2016 and 2017,31 % of global emissions, mostly from eastern China. We estimateemissions of 0.14 Gg yr−1 from northern and central India in 2016 andfind evidence for significant emissions from Russia. In contrast, recentemissions from northwestern Europe and Australia are estimated to be small(≤1 % each). We suggest that emissions from China, India, and Russiaare likely related to production of polytetrafluoroethylene (PTFE,“Teflon”) and other fluoropolymers and fluorochemicals that are based onthe pyrolysis of hydrochlorofluorocarbon HCFC-22 (CHClF2) in whichc-C4F8 is a known by-product. The semiconductor sector, wherec-C4F8 is used, is estimated to be a small source, at least inSouth Korea, Japan, Taiwan, and Europe. Without an obvious correlation withpopulation density, incineration of waste-containing fluoropolymers isprobably a minor source, and we find no evidence of emissions fromelectrolytic production of aluminum in Australia. While many possibleemissive uses of c-C4F8 are known and though we cannotcategorically exclude unknown sources, the start of significant emissionsmay well be related to the advent of commercial PTFE production in 1947.Process controls or abatement to reduce the c-C4F8 by-product wereprobably not in place in the early decades, explaining the increase inemissions in the 1960s and 1970s. With the advent of by-product reportingrequirements to the United Nations Framework Convention on Climate Change(UNFCCC) in the 1990s, concern about climate change and product stewardship,abatement, and perhaps the collection of c-C4F8 by-product for usein the semiconductor industry where it can be easily abated, it isconceivable that emissions in developed countries were stabilized and thenreduced, explaining the observed emission reduction in the 1980s and 1990s.Concurrently, production of PTFE in China began to increase rapidly. Withoutemission reduction requirements, it is plausible that global emissions todayare dominated by China and other developing countries. We predict thatc-C4F8 emissions will continue to rise and that c-C4F8will become the second most important emitted PFC in terms ofCO2-equivalent emissions within a year or two. The 2017 radiativeforcing of c-C4F8 (0.52 mW m−2) is small but emissions ofc-C4F8 and other PFCs, due to their very long atmosphericlifetimes, essentially permanently alter Earth's radiative budget and shouldbe reduced. Significant emissions inferred outside of the investigatedregions clearly show that observational capabilities and reportingrequirements need to be improved to understand global and country-scaleemissions of PFCs and other synthetic greenhouse gases and ozone-depletingsubstances.

Published
2019

10. Optically detected magnetic resonance of nitrogen vacancies in a diamond anvil cell using designer diamond anvils

Author

Steele, L., Lawson, M., Onyszczak, M., Bush, B. T., Mei, Z., Dioguardi, A. P., King, J., Parker, A., Pines, A., Weir, S. T., Evans, W., Visbeck, K., Vohra, Y. K., and Curro, N. J.

Subjects
Physics - Instrumentation and Detectors, Condensed Matter - Strongly Correlated Electrons
Abstract

Optically detected magnetic resonance of nitrogen vacancy centers in diamond offers novel routes to both DC and AC magnetometry in diamond anvil cells under high pressures ($>3$ GPa). However, a serious challenge to realizing experiments has been the insertion of microwave radiation in to the sample space without screening by the gasket material. We utilize designer anvils with lithographically-deposited metallic microchannels on the diamond culet as a microwave antenna. We detected the spin resonance of an ensemble of microdiamonds under pressure, and measure the pressure dependence of the zero field splitting parameters. These experiments enable the possibility for all-optical magnetic resonance experiments on sub-$\mu$L sample volumes at high pressures., Comment: 7 pages, 4 figures

Published
2017
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12. Boston biorepository, recruitment and integrative network (BBRAIN): A resource for the Gulf War Illness scientific community

Author

Keating, D., Zundel, C.G., Abreu, M., Krengel, M., Aenlle, K., Nichols, M.D., Toomey, R., Chao, L.L., Golier, J., Abdullah, L., Quinn, E., Heeren, T., Groh, J.R., Koo, B.B., Killiany, R., Loggia, M.L., Younger, J., Baraniuk, J., Janulewicz, P., Ajama, J., Quay, M., Baas, P.W., Qiang, L., Conboy, L., Kokkotou, E., O'Callaghan, J.P., Steele, L., Klimas, N., and Sullivan, K.

Published
2021
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13. Role of atmospheric oxidation in recent methane growth

Author

Rigby, Matthew, Montzka, Stephen A, Prinn, Ronald G, White, James WC, Young, Dickon, O’Doherty, Simon, Lunt, Mark F, Ganesan, Anita L, Manning, Alistair J, Simmonds, Peter G, Salameh, Peter K, Harth, Christina M, Mühle, Jens, Weiss, Ray F, Fraser, Paul J, Steele, L Paul, Krummel, Paul B, McCulloch, Archie, and Park, Sunyoung

Subjects
methane, hydroxyl, inversion, methyl chloroform, 1, 1, 1-trichloroethane
Abstract

The growth in global methane (CH4) concentration, which had been ongoing since the industrial revolution, stalled around the year 2000 before resuming globally in 2007. We evaluate the role of the hydroxyl radical (OH), the major CH4 sink, in the recent CH4 growth. We also examine the influence of systematic uncertainties in OH concentrations on CH4 emissions inferred from atmospheric observations. We use observations of 1,1,1-trichloroethane (CH3CCl3), which is lost primarily through reaction with OH, to estimate OH levels as well as CH3CC3 emissions, which have uncertainty that previously limited the accuracy of OH estimates. We find a 64-70% probability that a decline in OH has contributed to the post-2007 methane rise. Our median solution suggests that CH4 emissions increased relatively steadily during the late 1990s and early 2000s, after which growth was more modest. This solution obviates the need for a sudden statistically significant change in total CH4 emissions around the year 2007 to explain the atmospheric observations and can explain some of the decline in the atmospheric 13CH4/12CH4 ratio and the recent growth in C2H6 Our approach indicates that significant OH-related uncertainties in the CH4 budget remain, and we find that it is not possible to implicate, with a high degree of confidence, rapid global CH4 emissions changes as the primary driver of recent trends when our inferred OH trends and these uncertainties are considered.

Published
2017

16. Reconciling reported and unreported HFC emissions with atmospheric observations

Author

Lunt, Mark F, Rigby, Matthew, Ganesan, Anita L, Manning, Alistair J, Prinn, Ronald G, O’Doherty, Simon, Mühle, Jens, Harth, Christina M, Salameh, Peter K, Arnold, Tim, Weiss, Ray F, Saito, Takuya, Yokouchi, Yoko, Krummel, Paul B, Steele, L Paul, Fraser, Paul J, Li, Shanlan, Park, Sunyoung, Reimann, Stefan, Vollmer, Martin K, Lunder, Chris, Hermansen, Ove, Schmidbauer, Norbert, Maione, Michela, Arduini, Jgor, Young, Dickon, and Simmonds, Peter G

Subjects
Climate Action, halocarbons, radiative forcing, climate change
Abstract

We infer global and regional emissions of five of the most abundant hydrofluorocarbons (HFCs) using atmospheric measurements from the Advanced Global Atmospheric Gases Experiment and the National Institute for Environmental Studies, Japan, networks. We find that the total CO2-equivalent emissions of the five HFCs from countries that are required to provide detailed, annual reports to the United Nations Framework Convention on Climate Change (UNFCCC) increased from 198 (175-221) Tg-CO2-eq ⋅ y(-1) in 2007 to 275 (246-304) Tg-CO2-eq ⋅ y(-1) in 2012. These global warming potential-weighted aggregated emissions agree well with those reported to the UNFCCC throughout this period and indicate that the gap between reported emissions and global HFC emissions derived from atmospheric trends is almost entirely due to emissions from nonreporting countries. However, our measurement-based estimates of individual HFC species suggest that emissions, from reporting countries, of the most abundant HFC, HFC-134a, were only 79% (63-95%) of the UNFCCC inventory total, while other HFC emissions were significantly greater than the reported values. These results suggest that there are inaccuracies in the reporting methods for individual HFCs, which appear to cancel when aggregated together.

Published
2015

17. Concentrations and isotope ratios of helium and other noble gases in the Earth's atmosphere during 1978-2011

Author

Brennwald, Matthias S., Vogel, Nadia, Figura, Simon, Vollmer, Martin K., Langenfelds, Ray, Steele, L. Paul, and Kipfer, Rolf

Subjects
Physics - Atmospheric and Oceanic Physics, Physics - Geophysics
Abstract

The evolution of the atmospheric noble gas composition during the past few decades has hardly been studied because, in contrast to many other atmospheric gases, systematic time-series measurements have not been available. Based on theoretical considerations, the atmospheric noble gas isotope composition is assumed to be stable on time scales of up to about 10^6 years, with the potential exception of anthropogenic changes predicted for the He concentration and the 3He/4He ratio. However, experimental assessments of the predicted changes in the atmospheric He isotope composition are controversial. To empirically test these assumptions and predictions, we analysed the noble gas isotope composition in samples of the Cape Grim Air Archive, a well-defined archive of marine boundary layer air in the southern hemisphere. The resulting time series of the 20Ne, 40Ar, 86Kr and 136Xe concentrations and 20Ne/22Ne and 40Ar/36Ar ratios during 1978-2011 demonstrate the stability of the atmospheric Ne, Ar, Kr and Xe composition during this time interval. The He isotope data provide strong evidence for a decrease in the 3He/4He during the same time interval at a mean rate of 0.23-0.30 permil per year. This result is consistent with most model predictions of the rate of decrease in the atmospheric 3He/4He ratio associated with mining and burning of fossil fuels.

Published
2012
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18. Three decades of global methane sources and sinks

Author

Kirschke, Stefanie, Bousquet, Philippe, Ciais, Philippe, Saunois, Marielle, Canadell, Josep G, Dlugokencky, Edward J, Bergamaschi, Peter, Bergmann, Daniel, Blake, Donald R, Bruhwiler, Lori, Cameron-Smith, Philip, Castaldi, Simona, Chevallier, Frédéric, Feng, Liang, Fraser, Annemarie, Heimann, Martin, Hodson, Elke L, Houweling, Sander, Josse, Béatrice, Fraser, Paul J, Krummel, Paul B, Lamarque, Jean-François, Langenfelds, Ray L, Le Quéré, Corinne, Naik, Vaishali, O'Doherty, Simon, Palmer, Paul I, Pison, Isabelle, Plummer, David, Poulter, Benjamin, Prinn, Ronald G, Rigby, Matt, Ringeval, Bruno, Santini, Monia, Schmidt, Martina, Shindell, Drew T, Simpson, Isobel J, Spahni, Renato, Steele, L Paul, Strode, Sarah A, Sudo, Kengo, Szopa, Sophie, van der Werf, Guido R, Voulgarakis, Apostolos, van Weele, Michiel, Weiss, Ray F, Williams, Jason E, and Zeng, Guang

Subjects
Climate Action, Meteorology & Atmospheric Sciences
Abstract

Methane is an important greenhouse gas, responsible for about 20% of the warming induced by long-lived greenhouse gases since pre-industrial times. By reacting with hydroxyl radicals, methane reduces the oxidizing capacity of the atmosphere and generates ozone in the troposphere. Although most sources and sinks of methane have been identified, their relative contributions to atmospheric methane levels are highly uncertain. As such, the factors responsible for the observed stabilization of atmospheric methane levels in the early 2000s, and the renewed rise after 2006, remain unclear. Here, we construct decadal budgets for methane sources and sinks between 1980 and 2010, using a combination of atmospheric measurements and results from chemical transport models, ecosystem models, climate chemistry models and inventories of anthropogenic emissions. The resultant budgets suggest that data-driven approaches and ecosystem models overestimate total natural emissions. We build three contrasting emission scenarios-which differ in fossil fuel and microbial emissions-to explain the decadal variability in atmospheric methane levels detected, here and in previous studies, since 1985. Although uncertainties in emission trends do not allow definitive conclusions to be drawn, we show that the observed stabilization of methane levels between 1999 and 2006 can potentially be explained by decreasing-to-stable fossil fuel emissions, combined with stable-to-increasing microbial emissions. We show that a rise in natural wetland emissions and fossil fuel emissions probably accounts for the renewed increase in global methane levels after 2006, although the relative contribution of these two sources remains uncertain. © 2013 Macmillan Publishers Limited.

Published
2013

19. Results from the International Halocarbons in Air Comparison Experiment (IHALACE)

Author

Hall, B. D, Engel, A., Mühle, J., Elkins, J. W, Artuso, F., Atlas, E., Aydin, M., Blake, D., Brunke, E.-G., Chiavarini, S., Fraser, P. J, Happell, J., Krummel, P. B, Levin, I., Loewenstein, M., Maione, M., Montzka, S. A, O'Doherty, S., Reimann, S., Rhoderick, G., Saltzman, E. S, Scheel, H. E, Steele, L. P, Vollmer, M. K, Weiss, R. F, Worthy, D., and Yokouchi, Y.

Subjects
international comparison, climate change, halocarbons, atmospheric measurements
Abstract

The International Halocarbons in Air Comparison Experiment (IHALACE) was conducted to document relationships between calibration scales among various laboratories that measure atmospheric greenhouse and ozone depleting gases. Six stainless steel cylinders containing natural and modified natural air samples were circulated among 19 laboratories. Results from this experiment reveal relatively good agreement among commonly used calibration scales for a number of trace gases present in the unpolluted atmosphere at pmol mol−1 (parts per trillion) levels, such as chlorofluorocarbons (CFCs), hydrochlorofluorocarbons (HCFCs), and hydrofluorocarbons (HFCs). Some scale relationships were found to be consistent with those derived from bi-lateral experiments or from analysis of atmospheric data, while others revealed discrepancies. The transfer of calibration scales among laboratories was found to be problematic in many cases, meaning that measurements tied to a common scale may not, in fact, be compatible. These results reveal substantial improvements in calibration over previous comparisons. However there is room for improvement in communication and coordination of calibration activities with respect to the measurement of halogenated and related trace gases.

Published
2013

20. A KRAS variant is a biomarker of poor outcome, platinum chemotherapy resistance and a potential target for therapy in ovarian cancer

Author

Ratner, ES, Keane, FK, Lindner, R, Tassi, RA, Paranjape, T, Glasgow, M, Nallur, S, Deng, Y, Lu, L, Steele, L, Sand, S, Muller, R-U, Bignotti, E, Bellone, S, Boeke, M, Yao, X, Pecorelli, S, Ravaggi, A, Katsaros, D, Zelterman, D, Cristea, MC, Yu, H, Rutherford, TJ, Weitzel, JN, Neuhausen, SL, Schwartz, PE, Slack, FJ, Santin, AD, and Weidhaas, JB

Subjects
Ovarian Cancer, Genetics, Rare Diseases, Clinical Research, Cancer, 2.1 Biological and endogenous factors, Aetiology, 3' Untranslated Regions, Aged, Antineoplastic Combined Chemotherapy Protocols, BRCA1 Protein, BRCA2 Protein, Biomarkers, Tumor, Carboplatin, Cell Line, Tumor, Cell Survival, Drug Resistance, Neoplasm, Female, Genotype, Humans, Kaplan-Meier Estimate, Middle Aged, Multivariate Analysis, Mutation, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, Paclitaxel, Polymorphism, Single Nucleotide, Prognosis, Proto-Oncogene Proteins, Proto-Oncogene Proteins p21(ras), RNA Interference, Treatment Outcome, ras Proteins, platinum resistance, KRAS variant, ovarian cancer, outcome, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Germline variants in the 3' untranslated region (3'UTR) of cancer genes disrupting microRNA (miRNA) regulation have recently been associated with cancer risk. A variant in the 3'UTR of the KRAS oncogene, referred to as the KRAS variant, is associated with both cancer risk and altered tumor biology. Here, we test the hypothesis that the KRAS variant can act as a biomarker of outcome in epithelial ovarian cancer (EOC), and investigate the cause of altered outcome in KRAS variant-positive EOC patients. As this variant seems to be associated with tumor biology, we additionally test the hypothesis that this variant can be directly targeted to impact cell survival. EOC patients with complete clinical data were genotyped for the KRAS variant and analyzed for outcome (n=536), response to neoadjuvant chemotherapy (n=125) and platinum resistance (n=306). Outcome was separately analyzed for women with known BRCA mutations (n=79). Gene expression was analyzed on a subset of tumors with available tissue. Cell lines were used to confirm altered sensitivity to chemotherapy associated with the KRAS variant. Finally, the KRAS variant was directly targeted through small-interfering RNA/miRNA oligonucleotides in cell lines and survival was measured. Postmenopausal EOC patients with the KRAS variant were significantly more likely to die of ovarian cancer by multivariate analysis (hazard ratio=1.67, 95% confidence interval: 1.09-2.57, P=0.019, n=279). Perhaps explaining this finding, EOC patients with the KRAS variant were significantly more likely to be platinum resistant (odds ratio=3.18, confidence interval: 1.31-7.72, P=0.0106, n=291). In addition, direct targeting of the KRAS variant led to a significant reduction in EOC cell growth and survival in vitro. These findings confirm the importance of the KRAS variant in EOC, and indicate that the KRAS variant is a biomarker of poor outcome in EOC likely due to platinum resistance. In addition, this study supports the hypothesis that these tumors have continued dependence on such 3'UTR lesions, and that direct targeting may be a viable future treatment approach.

Published
2012

21. Introduction to the Symposium – Decarcerating Disability, Criminal Justice and Law: New Writing on Disability, Abolition and the Limits of Rights

Author

Ben-Moshe, L and Steele, L

Abstract

Liat Ben-Moshe and Linda Steele introduce a Symposium on their 2020 publications Decarcerating Disability: Deinstitutionalization and Prison Abolition (Ben-Moshe) and Disability, Criminal Justice and Law: Reconsidering Court Diversion (Steele). Ben-Moshe and Steele introduce their own books and then identify connections between the books. They situate their discussion in the anti-carceral activism that emerged during 2020 and in longer term activist and scholarly work on deinstitutionalisation, prison abolition and rights in the criminal justice system.

Published
2023

22. Contraceptive use and the risk of ovarian cancer among women with a BRCA1 or BRCA2 mutation

Author

Xia, Y, Gronwald, J, Karlan, B, Lubinski, J, Mccuaig, J, Brooks, J, Moller, P, Eisen, A, Sun, S, Senter, L, Bordeleau, L, Neuhausen, S, Singer, C, Tung, N, Foulkes, W, Sun, P, Narod, S, Kotsopoulos, J, Yerushalmi, R, Fruscio, R, Rastelli, A, Zovato, S, Hyder, Z, Huzarski, T, Cybulski, C, Sweet, K, Wood, M, Mckinnon, W, Elser, C, Pal, T, Wiesner, G, Friedman, E, Meschino, W, Snyder, C, Metcalfe, K, Poll, A, Gojska, N, Warner, E, Kim, R, Rosen, B, Demsky, R, Ainsworth, P, Panabaker, K, Steele, L, Saal, H, Serfas, K, Panchal, S, Cullinane, A, Reilly, R, Blum, J, Kwong, A, Rayson, D, Isaacs, C, Ramón y Cajal, T, Dungan, J, Cohen, S, Xia Y. Y., Gronwald J., Karlan B., Lubinski J., McCuaig J. M., Brooks J., Moller P., Eisen A., Sun S., Senter L., Bordeleau L., Neuhausen S. L., Singer C. F., Tung N., Foulkes W. D., Sun P., Narod S. A., Kotsopoulos J., Yerushalmi R., Fruscio R., Rastelli A., Zovato S, Hyder Z., Huzarski T., Cybulski C, Sweet K., Wood M., McKinnon W., Elser C., Pal T., Wiesner G., Friedman E., Meschino W., Snyder C., Metcalfe K., Poll A., Gojska N., Warner E., Kim R. H., Rosen B., Demsky R., Ainsworth P., Panabaker K., Steele L., Saal H., Serfas K., Panchal S., Cullinane A., Reilly R. E., Blum J. L., Kwong A., Cybulski C., Rayson D., Isaacs C., Ramón y Cajal T., Dungan J., Cohen S., Xia, Y, Gronwald, J, Karlan, B, Lubinski, J, Mccuaig, J, Brooks, J, Moller, P, Eisen, A, Sun, S, Senter, L, Bordeleau, L, Neuhausen, S, Singer, C, Tung, N, Foulkes, W, Sun, P, Narod, S, Kotsopoulos, J, Yerushalmi, R, Fruscio, R, Rastelli, A, Zovato, S, Hyder, Z, Huzarski, T, Cybulski, C, Sweet, K, Wood, M, Mckinnon, W, Elser, C, Pal, T, Wiesner, G, Friedman, E, Meschino, W, Snyder, C, Metcalfe, K, Poll, A, Gojska, N, Warner, E, Kim, R, Rosen, B, Demsky, R, Ainsworth, P, Panabaker, K, Steele, L, Saal, H, Serfas, K, Panchal, S, Cullinane, A, Reilly, R, Blum, J, Kwong, A, Rayson, D, Isaacs, C, Ramón y Cajal, T, Dungan, J, Cohen, S, Xia Y. Y., Gronwald J., Karlan B., Lubinski J., McCuaig J. M., Brooks J., Moller P., Eisen A., Sun S., Senter L., Bordeleau L., Neuhausen S. L., Singer C. F., Tung N., Foulkes W. D., Sun P., Narod S. A., Kotsopoulos J., Yerushalmi R., Fruscio R., Rastelli A., Zovato S, Hyder Z., Huzarski T., Cybulski C, Sweet K., Wood M., McKinnon W., Elser C., Pal T., Wiesner G., Friedman E., Meschino W., Snyder C., Metcalfe K., Poll A., Gojska N., Warner E., Kim R. H., Rosen B., Demsky R., Ainsworth P., Panabaker K., Steele L., Saal H., Serfas K., Panchal S., Cullinane A., Reilly R. E., Blum J. L., Kwong A., Cybulski C., Rayson D., Isaacs C., Ramón y Cajal T., Dungan J., and Cohen S.

Abstract

Background BRCA1 and BRCA2 (BRCA) mutation carriers face a high lifetime risk of developing ovarian cancer. Oral contraceptives are protective in this population; however, the impact of other types of contraception (e.g. intrauterine devices, implants, injections) is unknown. We undertook a matched case-control study to evaluate the relationship between type of contraception and risk of ovarian cancer among women with BRCA mutations. Methods A total of 1733 matched pairs were included in this analysis. Women were matched according to year of birth, date of study entry, country of residence, BRCA mutation type and history of breast cancer. Detailed information on hormonal, reproductive and lifestyle exposures were collected from a routinely administered questionnaire. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) associated with each contraceptive exposure. Results Ever use of any contraceptive was significantly associated with reduced risk of ovarian cancer (OR = 0.62; 95% CI 0.52–0.75; P < 0.0001), which was driven by significant inverse associations with oral contraceptives (OR = 0.66; 95% CI 0.54–0.79; P < 0.0001) and contraceptive implants (OR = 0.30; 95% CI 0.12–0.73; P = 0.008). We observed a similar effect with use of injections (OR = 0.37; 95% CI 0.10–1.38; P = 0.14), but this did not achieve significance. No significant associations were observed between patterns of intrauterine device use and risk of ovarian cancer. Conclusions These findings support a protective effect of oral contraceptives and implants on risk of ovarian cancer among women with BRCA mutations. The possible protective effect of injections requires further evaluation.

Published
2022

26. Menstrual Justice: A Human Rights Vision for Australia

Author

Armour, M, Barrington, D, Connolly, H, Goldblatt, B, Hill, E, Howe, D, Johnson, ME, King, M, Lansbury, N, Nash, M, Steele, L, Ussher, JM, Armour, M, Barrington, D, Connolly, H, Goldblatt, B, Hill, E, Howe, D, Johnson, ME, King, M, Lansbury, N, Nash, M, Steele, L, and Ussher, JM

Published
2023

27. CCNE1 and survival of patients with tubo-ovarian high-grade serous carcinoma: An Ovarian Tumor Tissue Analysis consortium study

Author

Kang, E-Y, Weir, A, Meagher, NS, Farrington, K, Nelson, GS, Ghatage, P, Lee, C-H, Riggan, MJ, Bolithon, A, Popovic, G, Leung, B, Tang, K, Lambie, N, Millstein, J, Alsop, J, Anglesio, MS, Ataseven, B, Barlow, E, Beckmann, MW, Berger, J, Bisinotto, C, Boesmueller, H, Boros, J, Brand, AH, Brooks-Wilson, A, Brucker, SY, Carney, ME, Casablanca, Y, Cazorla-Jimenez, A, Cohen, PA, Conrads, TP, Cook, LS, Coulson, P, Courtney-Brooks, M, Cramer, DW, Crowe, P, Cunningham, JM, Cybulski, C, Darcy, KM, El-Bahrawy, MA, Elishaev, E, Erber, R, Farrell, R, Fereday, S, Fischer, A, Garcia, MJ, Gayther, SA, Gentry-Maharaj, A, Gilks, CB, Grube, M, Harnett, PR, Harrington, SP, Harter, P, Hartmann, A, Hecht, JL, Heikaus, S, Hein, A, Heitz, F, Hendley, J, Hernandez, BY, Hernando Polo, S, Heublein, S, Hirasawa, A, Hogdall, E, Hogdall, CK, Horlings, HM, Huntsman, DG, Huzarski, T, Jewell, A, Jimenez-Linan, M, Jones, ME, Kaufmann, SH, Kennedy, CJ, Khabele, D, Kommoss, FKF, Kruitwagen, RFPM, Lambrechts, D, Le, ND, Lener, M, Lester, J, Leung, Y, Linder, A, Loverix, L, Lubinski, J, Madan, R, Maxwell, GL, Modugno, F, Neuhausen, SL, Olawaiye, A, Olbrecht, S, Orsulic, S, Palacios, J, Pearce, CL, Pike, MC, Quinn, CM, Mohan, GR, Rodriguez-Antona, C, Ruebner, M, Ryan, A, Salfinger, SG, Sasamoto, N, Schildkraut, JM, Schoemaker, MJ, Shah, M, Sharma, R, Shvetsov, YB, Singh, N, Sonke, GS, Steele, L, Stewart, CJR, Sundfeldt, K, Swerdlow, AJ, Talhouk, A, Tan, A, Taylor, SE, Terry, KL, Toloczko, A, Traficante, N, Van de Vijver, KK, van der Aa, MA, Van Gorp, T, Van Nieuwenhuysen, E, Van-Wagensveld, L, Vergote, I, Vierkant, RA, Wang, C, Wilkens, LR, Winham, SJ, Wu, AH, Benitez, J, Berchuck, A, Candido Dos Reis, FJ, DeFazio, A, Fasching, PA, Goode, EL, Goodman, MT, Gronwald, J, Karlan, BY, Kommoss, S, Menon, U, Sinn, H-P, Staebler, A, Brenton, JD, Bowtell, DD, Pharoah, PDP, Ramus, SJ, Kobel, M, Kang, E-Y, Weir, A, Meagher, NS, Farrington, K, Nelson, GS, Ghatage, P, Lee, C-H, Riggan, MJ, Bolithon, A, Popovic, G, Leung, B, Tang, K, Lambie, N, Millstein, J, Alsop, J, Anglesio, MS, Ataseven, B, Barlow, E, Beckmann, MW, Berger, J, Bisinotto, C, Boesmueller, H, Boros, J, Brand, AH, Brooks-Wilson, A, Brucker, SY, Carney, ME, Casablanca, Y, Cazorla-Jimenez, A, Cohen, PA, Conrads, TP, Cook, LS, Coulson, P, Courtney-Brooks, M, Cramer, DW, Crowe, P, Cunningham, JM, Cybulski, C, Darcy, KM, El-Bahrawy, MA, Elishaev, E, Erber, R, Farrell, R, Fereday, S, Fischer, A, Garcia, MJ, Gayther, SA, Gentry-Maharaj, A, Gilks, CB, Grube, M, Harnett, PR, Harrington, SP, Harter, P, Hartmann, A, Hecht, JL, Heikaus, S, Hein, A, Heitz, F, Hendley, J, Hernandez, BY, Hernando Polo, S, Heublein, S, Hirasawa, A, Hogdall, E, Hogdall, CK, Horlings, HM, Huntsman, DG, Huzarski, T, Jewell, A, Jimenez-Linan, M, Jones, ME, Kaufmann, SH, Kennedy, CJ, Khabele, D, Kommoss, FKF, Kruitwagen, RFPM, Lambrechts, D, Le, ND, Lener, M, Lester, J, Leung, Y, Linder, A, Loverix, L, Lubinski, J, Madan, R, Maxwell, GL, Modugno, F, Neuhausen, SL, Olawaiye, A, Olbrecht, S, Orsulic, S, Palacios, J, Pearce, CL, Pike, MC, Quinn, CM, Mohan, GR, Rodriguez-Antona, C, Ruebner, M, Ryan, A, Salfinger, SG, Sasamoto, N, Schildkraut, JM, Schoemaker, MJ, Shah, M, Sharma, R, Shvetsov, YB, Singh, N, Sonke, GS, Steele, L, Stewart, CJR, Sundfeldt, K, Swerdlow, AJ, Talhouk, A, Tan, A, Taylor, SE, Terry, KL, Toloczko, A, Traficante, N, Van de Vijver, KK, van der Aa, MA, Van Gorp, T, Van Nieuwenhuysen, E, Van-Wagensveld, L, Vergote, I, Vierkant, RA, Wang, C, Wilkens, LR, Winham, SJ, Wu, AH, Benitez, J, Berchuck, A, Candido Dos Reis, FJ, DeFazio, A, Fasching, PA, Goode, EL, Goodman, MT, Gronwald, J, Karlan, BY, Kommoss, S, Menon, U, Sinn, H-P, Staebler, A, Brenton, JD, Bowtell, DD, Pharoah, PDP, Ramus, SJ, and Kobel, M

Abstract

BACKGROUND: Cyclin E1 (CCNE1) is a potential predictive marker and therapeutic target in tubo-ovarian high-grade serous carcinoma (HGSC). Smaller studies have revealed unfavorable associations for CCNE1 amplification and CCNE1 overexpression with survival, but to date no large-scale, histotype-specific validation has been performed. The hypothesis was that high-level amplification of CCNE1 and CCNE1 overexpression, as well as a combination of the two, are linked to shorter overall survival in HGSC. METHODS: Within the Ovarian Tumor Tissue Analysis consortium, amplification status and protein level in 3029 HGSC cases and mRNA expression in 2419 samples were investigated. RESULTS: High-level amplification (>8 copies by chromogenic in situ hybridization) was found in 8.6% of HGSC and overexpression (>60% with at least 5% demonstrating strong intensity by immunohistochemistry) was found in 22.4%. CCNE1 high-level amplification and overexpression both were linked to shorter overall survival in multivariate survival analysis adjusted for age and stage, with hazard stratification by study (hazard ratio [HR], 1.26; 95% CI, 1.08-1.47, p = .034, and HR, 1.18; 95% CI, 1.05-1.32, p = .015, respectively). This was also true for cases with combined high-level amplification/overexpression (HR, 1.26; 95% CI, 1.09-1.47, p = .033). CCNE1 mRNA expression was not associated with overall survival (HR, 1.00 per 1-SD increase; 95% CI, 0.94-1.06; p = .58). CCNE1 high-level amplification is mutually exclusive with the presence of germline BRCA1/2 pathogenic variants and shows an inverse association to RB1 loss. CONCLUSION: This study provides large-scale validation that CCNE1 high-level amplification is associated with shorter survival, supporting its utility as a prognostic biomarker in HGSC.

Published
2023

28. Disability activism and institutional heritage

Author

Carnemolla, P, Steele, L, Carnemolla, P, and Steele, L

Abstract

This article focuses on former sites of disability institutions and activism of people with disability. It argues that planning processes for redevelopment and re-use of sites of former institutions are an important focus for activism, particularly for reparative urban planning and inclusive community engagement. This argument is made through two sets of data. First, disability activism is explored in a case study of the 2021 New South Wales (Australia) Government planning proposal for rezoning Peat Island. The proposal overlooked the island’s 99-year history as an institution and excluded people with intellectual disability from engaging in planning processes. Second, the article contextualises the Peat Island case study within the authors’ empirical research with people with intellectual disability about remembering institutions. Together, these sets of data underscore links between disability history and futures by bringing together institutional heritage and urban planning with recognition of lived experiences (including activism) of people who were institutionalised. This historical context is then considered alongside present-day disability activism for a more inclusive, equitable future. The article proposes further research on disability-inclusive, reparative planning approaches to redevelopment and re-use of former sites of institutions to promote disability activist leadership and contributions to the afterlives of former institutions.

Published
2023

29. Listening to People with Intellectual Disability about Institutions

Author

Steele, L, Carnemolla, P, Spencer, R, Kelly, J, Naing, L, Dowse, L, Steele, L, Carnemolla, P, Spencer, R, Kelly, J, Naing, L, and Dowse, L

Abstract

Despite the ongoing impacts worldwide of institutionalisation on people with intellectual disability, the public knows little about large-scale disability institutions that have been the focus during the late 20th century of deinstitutionalisation efforts (historic institutions) and the people who lived there. An interdisciplinary team of researchers (including those with intellectual disability) undertook research with people with intellectual disability to explore what and how the public should learn and remember historic institutions. The project found that people with intellectual disability support community engagement with histories and lived experiences of historic institutions, in order to repair past wrongs, end contemporary practices of institutionalisation, segregation, and exclusion, and realise transformative equality and inclusion. People with intellectual disability should lead these initiatives, with appropriate support in recognising the very live memories and traumas associated with them. This article provides a model of inclusive research for turning the harms of past institutionalisation into an educational and reparative experience.

Published
2023

30. Characterizing prostate cancer risk through multi-ancestry genome-wide discovery of 187 novel risk variants.

Author

Wang, A, Shen, J, Rodriguez, AA, Saunders, EJ, Chen, F, Janivara, R, Darst, BF, Sheng, X, Xu, Y, Chou, AJ, Benlloch, S, Dadaev, T, Brook, MN, Plym, A, Sahimi, A, Hoffman, TJ, Takahashi, A, Matsuda, K, Momozawa, Y, Fujita, M, Laisk, T, Figuerêdo, J, Muir, K, Ito, S, Liu, X, Biobank Japan Project, Uchio, Y, Kubo, M, Kamatani, Y, Lophatananon, A, Wan, P, Andrews, C, Lori, A, Choudhury, PP, Schleutker, J, Tammela, TLJ, Sipeky, C, Auvinen, A, Giles, GG, Southey, MC, MacInnis, RJ, Cybulski, C, Wokolorczyk, D, Lubinski, J, Rentsch, CT, Cho, K, Mcmahon, BH, Neal, DE, Donovan, JL, Hamdy, FC, Martin, RM, Nordestgaard, BG, Nielsen, SF, Weischer, M, Bojesen, SE, Røder, A, Stroomberg, HV, Batra, J, Chambers, S, Horvath, L, Clements, JA, Tilly, W, Risbridger, GP, Gronberg, H, Aly, M, Szulkin, R, Eklund, M, Nordstrom, T, Pashayan, N, Dunning, AM, Ghoussaini, M, Travis, RC, Key, TJ, Riboli, E, Park, JY, Sellers, TA, Lin, H-Y, Albanes, D, Weinstein, S, Cook, MB, Mucci, LA, Giovannucci, E, Lindstrom, S, Kraft, P, Hunter, DJ, Penney, KL, Turman, C, Tangen, CM, Goodman, PJ, Thompson, IM, Hamilton, RJ, Fleshner, NE, Finelli, A, Parent, M-É, Stanford, JL, Ostrander, EA, Koutros, S, Beane Freeman, LE, Stampfer, M, Wolk, A, Håkansson, N, Andriole, GL, Hoover, RN, Machiela, MJ, Sørensen, KD, Borre, M, Blot, WJ, Zheng, W, Yeboah, ED, Mensah, JE, Lu, Y-J, Zhang, H-W, Feng, N, Mao, X, Wu, Y, Zhao, S-C, Sun, Z, Thibodeau, SN, McDonnell, SK, Schaid, DJ, West, CML, Barnett, G, Maier, C, Schnoeller, T, Luedeke, M, Kibel, AS, Drake, BF, Cussenot, O, Cancel-Tassin, G, Menegaux, F, Truong, T, Koudou, YA, John, EM, Grindedal, EM, Maehle, L, Khaw, K-T, Ingles, SA, Stern, MC, Vega, A, Gómez-Caamaño, A, Fachal, L, Rosenstein, BS, Kerns, SL, Ostrer, H, Teixeira, MR, Paulo, P, Brandão, A, Watya, S, Lubwama, A, Bensen, JT, Butler, EN, Mohler, JL, Taylor, JA, Kogevinas, M, Dierssen-Sotos, T, Castaño-Vinyals, G, Cannon-Albright, L, Teerlink, CC, Huff, CD, Pilie, P, Yu, Y, Bohlender, RJ, Gu, J, Strom, SS, Multigner, L, Blanchet, P, Brureau, L, Kaneva, R, Slavov, C, Mitev, V, Leach, RJ, Brenner, H, Chen, X, Holleczek, B, Schöttker, B, Klein, EA, Hsing, AW, Kittles, RA, Murphy, AB, Logothetis, CJ, Kim, J, Neuhausen, SL, Steele, L, Ding, YC, Isaacs, WB, Nemesure, B, Hennis, AJM, Carpten, J, Pandha, H, Michael, A, De Ruyck, K, De Meerleer, G, Ost, P, Xu, J, Razack, A, Lim, J, Teo, S-H, Newcomb, LF, Lin, DW, Fowke, JH, Neslund-Dudas, CM, Rybicki, BA, Gamulin, M, Lessel, D, Kulis, T, Usmani, N, Abraham, A, Singhal, S, Parliament, M, Claessens, F, Joniau, S, Van den Broeck, T, Gago-Dominguez, M, Castelao, JE, Martinez, ME, Larkin, S, Townsend, PA, Aukim-Hastie, C, Bush, WS, Aldrich, MC, Crawford, DC, Srivastava, S, Cullen, J, Petrovics, G, Casey, G, Wang, Y, Tettey, Y, Lachance, J, Tang, W, Biritwum, RB, Adjei, AA, Tay, E, Truelove, A, Niwa, S, Yamoah, K, Govindasami, K, Chokkalingam, AP, Keaton, JM, Hellwege, JN, Clark, PE, Jalloh, M, Gueye, SM, Niang, L, Ogunbiyi, O, Shittu, O, Amodu, O, Adebiyi, AO, Aisuodionoe-Shadrach, OI, Ajibola, HO, Jamda, MA, Oluwole, OP, Nwegbu, M, Adusei, B, Mante, S, Darkwa-Abrahams, A, Diop, H, Gundell, SM, Roobol, MJ, Jenster, G, van Schaik, RHN, Hu, JJ, Sanderson, M, Kachuri, L, Varma, R, McKean-Cowdin, R, Torres, M, Preuss, MH, Loos, RJF, Zawistowski, M, Zöllner, S, Lu, Z, Van Den Eeden, SK, Easton, DF, Ambs, S, Edwards, TL, Mägi, R, Rebbeck, TR, Fritsche, L, Chanock, SJ, Berndt, SI, Wiklund, F, Nakagawa, H, Witte, JS, Gaziano, JM, Justice, AC, Mancuso, N, Terao, C, Eeles, RA, Kote-Jarai, Z, Madduri, RK, Conti, DV, Haiman, CA, Wang, A, Shen, J, Rodriguez, AA, Saunders, EJ, Chen, F, Janivara, R, Darst, BF, Sheng, X, Xu, Y, Chou, AJ, Benlloch, S, Dadaev, T, Brook, MN, Plym, A, Sahimi, A, Hoffman, TJ, Takahashi, A, Matsuda, K, Momozawa, Y, Fujita, M, Laisk, T, Figuerêdo, J, Muir, K, Ito, S, Liu, X, Biobank Japan Project, Uchio, Y, Kubo, M, Kamatani, Y, Lophatananon, A, Wan, P, Andrews, C, Lori, A, Choudhury, PP, Schleutker, J, Tammela, TLJ, Sipeky, C, Auvinen, A, Giles, GG, Southey, MC, MacInnis, RJ, Cybulski, C, Wokolorczyk, D, Lubinski, J, Rentsch, CT, Cho, K, Mcmahon, BH, Neal, DE, Donovan, JL, Hamdy, FC, Martin, RM, Nordestgaard, BG, Nielsen, SF, Weischer, M, Bojesen, SE, Røder, A, Stroomberg, HV, Batra, J, Chambers, S, Horvath, L, Clements, JA, Tilly, W, Risbridger, GP, Gronberg, H, Aly, M, Szulkin, R, Eklund, M, Nordstrom, T, Pashayan, N, Dunning, AM, Ghoussaini, M, Travis, RC, Key, TJ, Riboli, E, Park, JY, Sellers, TA, Lin, H-Y, Albanes, D, Weinstein, S, Cook, MB, Mucci, LA, Giovannucci, E, Lindstrom, S, Kraft, P, Hunter, DJ, Penney, KL, Turman, C, Tangen, CM, Goodman, PJ, Thompson, IM, Hamilton, RJ, Fleshner, NE, Finelli, A, Parent, M-É, Stanford, JL, Ostrander, EA, Koutros, S, Beane Freeman, LE, Stampfer, M, Wolk, A, Håkansson, N, Andriole, GL, Hoover, RN, Machiela, MJ, Sørensen, KD, Borre, M, Blot, WJ, Zheng, W, Yeboah, ED, Mensah, JE, Lu, Y-J, Zhang, H-W, Feng, N, Mao, X, Wu, Y, Zhao, S-C, Sun, Z, Thibodeau, SN, McDonnell, SK, Schaid, DJ, West, CML, Barnett, G, Maier, C, Schnoeller, T, Luedeke, M, Kibel, AS, Drake, BF, Cussenot, O, Cancel-Tassin, G, Menegaux, F, Truong, T, Koudou, YA, John, EM, Grindedal, EM, Maehle, L, Khaw, K-T, Ingles, SA, Stern, MC, Vega, A, Gómez-Caamaño, A, Fachal, L, Rosenstein, BS, Kerns, SL, Ostrer, H, Teixeira, MR, Paulo, P, Brandão, A, Watya, S, Lubwama, A, Bensen, JT, Butler, EN, Mohler, JL, Taylor, JA, Kogevinas, M, Dierssen-Sotos, T, Castaño-Vinyals, G, Cannon-Albright, L, Teerlink, CC, Huff, CD, Pilie, P, Yu, Y, Bohlender, RJ, Gu, J, Strom, SS, Multigner, L, Blanchet, P, Brureau, L, Kaneva, R, Slavov, C, Mitev, V, Leach, RJ, Brenner, H, Chen, X, Holleczek, B, Schöttker, B, Klein, EA, Hsing, AW, Kittles, RA, Murphy, AB, Logothetis, CJ, Kim, J, Neuhausen, SL, Steele, L, Ding, YC, Isaacs, WB, Nemesure, B, Hennis, AJM, Carpten, J, Pandha, H, Michael, A, De Ruyck, K, De Meerleer, G, Ost, P, Xu, J, Razack, A, Lim, J, Teo, S-H, Newcomb, LF, Lin, DW, Fowke, JH, Neslund-Dudas, CM, Rybicki, BA, Gamulin, M, Lessel, D, Kulis, T, Usmani, N, Abraham, A, Singhal, S, Parliament, M, Claessens, F, Joniau, S, Van den Broeck, T, Gago-Dominguez, M, Castelao, JE, Martinez, ME, Larkin, S, Townsend, PA, Aukim-Hastie, C, Bush, WS, Aldrich, MC, Crawford, DC, Srivastava, S, Cullen, J, Petrovics, G, Casey, G, Wang, Y, Tettey, Y, Lachance, J, Tang, W, Biritwum, RB, Adjei, AA, Tay, E, Truelove, A, Niwa, S, Yamoah, K, Govindasami, K, Chokkalingam, AP, Keaton, JM, Hellwege, JN, Clark, PE, Jalloh, M, Gueye, SM, Niang, L, Ogunbiyi, O, Shittu, O, Amodu, O, Adebiyi, AO, Aisuodionoe-Shadrach, OI, Ajibola, HO, Jamda, MA, Oluwole, OP, Nwegbu, M, Adusei, B, Mante, S, Darkwa-Abrahams, A, Diop, H, Gundell, SM, Roobol, MJ, Jenster, G, van Schaik, RHN, Hu, JJ, Sanderson, M, Kachuri, L, Varma, R, McKean-Cowdin, R, Torres, M, Preuss, MH, Loos, RJF, Zawistowski, M, Zöllner, S, Lu, Z, Van Den Eeden, SK, Easton, DF, Ambs, S, Edwards, TL, Mägi, R, Rebbeck, TR, Fritsche, L, Chanock, SJ, Berndt, SI, Wiklund, F, Nakagawa, H, Witte, JS, Gaziano, JM, Justice, AC, Mancuso, N, Terao, C, Eeles, RA, Kote-Jarai, Z, Madduri, RK, Conti, DV, and Haiman, CA

Abstract

The transferability and clinical value of genetic risk scores (GRSs) across populations remain limited due to an imbalance in genetic studies across ancestrally diverse populations. Here we conducted a multi-ancestry genome-wide association study of 156,319 prostate cancer cases and 788,443 controls of European, African, Asian and Hispanic men, reflecting a 57% increase in the number of non-European cases over previous prostate cancer genome-wide association studies. We identified 187 novel risk variants for prostate cancer, increasing the total number of risk variants to 451. An externally replicated multi-ancestry GRS was associated with risk that ranged from 1.8 (per standard deviation) in African ancestry men to 2.2 in European ancestry men. The GRS was associated with a greater risk of aggressive versus non-aggressive disease in men of African ancestry (P = 0.03). Our study presents novel prostate cancer susceptibility loci and a GRS with effective risk stratification across ancestry groups.

Published
2023

31. Law and Disability ‘Supported’ Employment in Australia: The Case for Ending Segregation, Discrimination, Exploitation and Violence of People with Disability at Work

Author

Steele, L and Steele, L

Abstract

This article argues for transition away from Australian Disability Enterprises (ADEs) on the basis that they further segregation, discrimination, exploitation, and violence against people with disability. ADEs (previously ‘sheltered workshops') overwhelmingly impact people with intellectual and cognitive disability. In ADEs, employees with disability receive less than award wages. They work in segregated settings where they are separate to and in unequal relationships with employees without disability. While sometimes framed as an opportunity for skills development, ADE employees with disability are unlikely to move into open employment. Currently, a variety of laws across diverse domains, including disability services law, industrial relations law and guardianship law, have justified ADEs as necessary and beneficial to people with disability and facilitated the organisations that operate ADEs receiving financial benefit from the unequal treatment of ADE employees with disability. Legal institutions with authority to help dismantle ADEs—Commonwealth legislature, the Fair Work Commission and Federal Court—have further entrenched ADEs in law by dismissing claims that they are harmful to people with disability. Ultimately, the article provides a basis for the need for law reform to transition away from ADEs in a broader context of enhancing dignity, equality and self-determination of people with disability.

Published
2023

33. Our Right to Decide: Equality and Autonomy for Women with Disability: Women with Disabilities Australia Submission on Guardianship and Financial Management to the Royal Commission into Violence, Abuse, Neglect and Exploitation of People with Disability

Author

Steele, L, Frohmader, C, Siciliano, H, Rose, E, Gosden-Kaye, E, Steele, L, Frohmader, C, Siciliano, H, Rose, E, and Gosden-Kaye, E

Abstract

In December 2022, WWDA submitted a response on guardianship and financial management to the Disability Royal Commission (DRC). Our response focuses on the equality and autonomy of women with disability. The response includes seventeen broad recommendations, which are prefaced by a clear call to action for the DRC: That the Disability Royal Commission must recognise that guardianship and financial management laws and other substitute-decision making regimes, continue to enable violence against women with disability and undermine their equality and autonomy. That the Disability Royal Commission must make recommendations for guardianship and financial management to be replaced with supported decision-making and other measures that facilitate disabled women’s equality and autonomy, including through deinstitutionalisation, desegregation, and reparations.

Published
2023

35. Ending disability segregated employment: ‘modern slavery’ law and disabled people's human right to work

Author

Steele, L and Steele, L

Abstract

Disability segregated employment (also referred to as ‘sheltered workshops’) violates disabled people’s human right to work and employment. This article argues that modern slavery law might serve as one part of a broader strategy to end disability segregated employment, ensure accountability for the injustices within them and ensure equal access to open employment opportunities for disabled people. This is on the basis that disability segregated employment can be understood as a form of labour exploitation under modern slavery law – specifically forced labour and servitude. Modern slavery law is a useful legal tool to unseat deeply entrenched ableist attitudes of disability segregated employment as beneficial and necessary and build corporate/charity, public and government momentum towards the transition away from disabil ity segregated employment, even if this particular area of law cannot itself legally compel the closure of sheltered workshops and an increase in open employment opportunities for disabled people.

Published
2023

40. Reparations for People Living with Dementia: Recognition, Accountability, Change, Now!

Author

Steele, L, Swaffer, K, Siciliano, H, Rose, E, Mitchell, W, Kobier, K, Bailey, B, Steele, L, Swaffer, K, Siciliano, H, Rose, E, Mitchell, W, Kobier, K, and Bailey, B

Abstract

There is a significant and longstanding problem of harm to people living with dementia in long term care institutions (‘LTC institutions’, referred to by others as ‘care homes’, ‘nursing homes’, ‘long term care’, ‘residential aged care facilities’), along with a failure to redress the harm or hold people accountable for this harm. This article reports on an Australian project that found reparations must be a response to harm to people living with dementia in residential aged care. Using a disability human rights methodology, focus groups were conducted with people living with dementia, care partners and family members, advocates and lawyers to explore perspectives on why and how to redress harm to people living with dementia in Australian LTC institutions. Researchers found four key themes provide the basis for the necessity and design of a reparative approach to redress – recognition, accountability, change, now. The article calls for further attention to reparations in dementia scholarship, with a particular focus on the role that can be played in the delivery of reparations by the LTC industry, dementia practitioners, and dementia scholars. Ultimately, this article provides a new understanding of responses to violence, abuse, neglect and other harms experienced by people living with dementia in LTC institutions, which centres justice, rights, and transformative change.

Published
2023

45. Three-dimensional model synthesis of the global methane cycle

Author

Fung, I., John, J., Lerner, J., Matthews, E., Prather, M., Steele, L. P, and Fraser, P. J

Subjects
atmospheric carbon-monoxide, general-circulation model, tropospheric methane, southern-hemisphere, spectroscopic measurements, isotopic composition, seasonal cycles, boundary-layer, rice paddies, tracer model
Abstract

The geographic and seasonal emission distributions of the major sources and sinks of atmospheric methane were compiled using methane flux measurements and energy and agricultural statistics in conjunction with global digital data bases of land surface characteristics and anthropogenic activities. Chemical destruction of methane in the atmosphere was calculated using three-dimensional OH fields every 5 days taken from Spivakovsky et al. (1990a, b). The signatures of each of the sources and sinks in the atmosphere were simulated using a global three-dimensional tracer transport model. Candidate methane budget scenarios were constructed according to mass balance of methane and its carbon isotopes. The verisimilitude of the scenarios was tested by their ability to reproduce the meridional gradient and seasonal variations of methane observed in the atmosphere. Constraints imposed by all the atmospheric observations are satisfied simultaneously by several budget scenarios. A preferred budget comprises annual destruction rates of 450 Tg by OH oxidation and 10 Tg by soil absorption and annual emissions of 80 Tg from fossil sources, 80 Tg from domestic animals, and 35 Tg from wetlands and tundra poleward of 50°N. Emissions from landfills, tropical swamps, rice fields, biomass burning, and termites total 295 Tg; however, the individual contributions of these terms cannot be determined uniquely because of the lack of measurements of direct fluxes and of atmospheric methane variations in regions where these sources are concentrated.

Published
1991

47. Breast cancer risk after age 60 among BRCA1 and BRCA2 mutation carriers

Author

Stjepanovic, N, Lubinski, J, Moller, P, Randall Armel, S, Foulkes, W, Tung, N, Neuhausen, S, Kotsopoulos, J, Sun, P, Sun, S, Eisen, A, Narod, S, Senter, L, Couch, C, Fruscio, R, Weitzel, J, Olopade, O, Singer, C, Pal, T, Huzarski, T, Cybulski, C, Sweet, K, Zakalik, D, Wood, M, Mckinnon, W, Elser, C, Wiesner, G, Friedman, E, Meschino, W, Snyder, C, Metcalfe, K, Poll, A, Warner, E, Kim, R, Demsky, R, Ainsworth, P, Steele, L, Saal, H, Serfas, K, Panchal, S, Cullinane, C, Reilly, R, Blum, J, Kwong, A, Rayson, D, Cajal, T, Dungan, J, Yerushalmi, R, Ginsburg, O, Schraeder, I, Cohen, S, Lemirelemire, E, Zovato, S, Rastelli, A, Gronwald, J, Mccuaig, J, Karlan, B, Bordeleau, L, Stjepanovic N., Lubinski J., Moller P., Randall Armel S., Foulkes W. D., Tung N., Neuhausen S. L., Kotsopoulos J., Sun P., Sun S., Eisen A., Narod S. A., Senter L., Couch C. E. F., Fruscio R., Weitzel J. N., Olopade O., Singer C. F., Pal T., Huzarski T., Cybulski C., Sweet K., Zakalik D., Wood M., McKinnon W., Elser C., Wiesner G., Friedman E., Meschino W., Snyder C., Metcalfe K., Poll A., Warner E., Kim R., Demsky R., Ainsworth P., Steele L., Saal H., Serfas K., Panchal S., Cullinane C. A., Reilly R. E., Blum J. L., Kwong A., Rayson D., Cajal T. R., Dungan J., Yerushalmi R., Ginsburg O., Schraeder I., Cohen S., LemireLemire E., Zovato S., Rastelli A., Gronwald J., McCuaig J., Karlan B., Bordeleau L., Stjepanovic, N, Lubinski, J, Moller, P, Randall Armel, S, Foulkes, W, Tung, N, Neuhausen, S, Kotsopoulos, J, Sun, P, Sun, S, Eisen, A, Narod, S, Senter, L, Couch, C, Fruscio, R, Weitzel, J, Olopade, O, Singer, C, Pal, T, Huzarski, T, Cybulski, C, Sweet, K, Zakalik, D, Wood, M, Mckinnon, W, Elser, C, Wiesner, G, Friedman, E, Meschino, W, Snyder, C, Metcalfe, K, Poll, A, Warner, E, Kim, R, Demsky, R, Ainsworth, P, Steele, L, Saal, H, Serfas, K, Panchal, S, Cullinane, C, Reilly, R, Blum, J, Kwong, A, Rayson, D, Cajal, T, Dungan, J, Yerushalmi, R, Ginsburg, O, Schraeder, I, Cohen, S, Lemirelemire, E, Zovato, S, Rastelli, A, Gronwald, J, Mccuaig, J, Karlan, B, Bordeleau, L, Stjepanovic N., Lubinski J., Moller P., Randall Armel S., Foulkes W. D., Tung N., Neuhausen S. L., Kotsopoulos J., Sun P., Sun S., Eisen A., Narod S. A., Senter L., Couch C. E. F., Fruscio R., Weitzel J. N., Olopade O., Singer C. F., Pal T., Huzarski T., Cybulski C., Sweet K., Zakalik D., Wood M., McKinnon W., Elser C., Wiesner G., Friedman E., Meschino W., Snyder C., Metcalfe K., Poll A., Warner E., Kim R., Demsky R., Ainsworth P., Steele L., Saal H., Serfas K., Panchal S., Cullinane C. A., Reilly R. E., Blum J. L., Kwong A., Rayson D., Cajal T. R., Dungan J., Yerushalmi R., Ginsburg O., Schraeder I., Cohen S., LemireLemire E., Zovato S., Rastelli A., Gronwald J., McCuaig J., Karlan B., and Bordeleau L.

Abstract

Purpose: It is not known whether the risk of breast cancer among BRCA1 and BRCA2 mutation carriers after age 60 is high enough to justify intensive screening or prophylactic surgery. Thus, we conducted a prospective analysis of breast cancer risk in BRCA1 and BRCA2 mutation carriers from age 60 until age 80. Methods: Subjects had no history of cancer and both breasts intact at age 60 (n = 699). Women were followed until a breast cancer diagnosis, prophylactic bilateral mastectomy or death. We calculated the annual cancer rate and cumulative incidence of breast cancer (invasive and in situ) from age 60 to age 80. We assessed the associations between hormone replacement therapy, family history of breast cancer and bilateral oophorectomy and breast cancer risk. Results: Over a mean follow-up of 7.9 years, 61 invasive and 20 in situ breast cancers were diagnosed in the cohort. The mean annual rate of invasive breast cancer was 1.8% for BRCA1 mutation carriers and 1.7% for BRCA2 mutation carriers. The cumulative risk of invasive breast cancer from age 60 to 80 was 20.1% for women with a BRCA1 mutation and was 17.3% for women with a BRCA2 mutation. Hormone replacement therapy, family history and oophorectomy were not associated with breast cancer risk. Conclusions: Findings from this large prospective study indicate that the risk of developing breast cancer remains high after age 60 in both BRCA1 and BRCA2 mutation carriers. These findings warrant further evaluation of the role of breast cancer screening in older mutation carriers.

Published
2021

48. Prospective, multicentre study of external ventricular drainage-related infections in the UK and Ireland

Author

Jamjoom, Aimun A B, Joannides, Alexis J, Poon, Michael Tin-Chung, Chari, Aswin, Zaben, Malik, Abdulla, Mutwakil A H, Roach, Joy, Glancz, Laurence J, Solth, Anna, Duddy, John, Brennan, Paul M, Bayston, Roger, Bulters, Diederik O, Mallucci, Conor L, Jenkinson, Michael D, Gray, William P, Kandasamy, Jothy, Hutchinson, Peter J, Kolias, Angelos G, Ahmed, Aminul I, Alalade, A, Bailey, M, Basu, S, Baudracco, I, Bhattacharya, A, Bodkin, Pa, Boissaud-cooke, M, Bojanic, S, Buxton, N, Corns, R, Coulter, C, Coulter, I, Critchley, G, Dando, A, Dardis, R, Dyson, E, Edwards, R, Garnett, M, Gatcher, S, Georges, H, Hallet, J, Harte, J, Haylock-vize, P, Humphreys, H, Kitchen, J, Lawson Mclean, A, Loan, JJM, Ma, R, Madder, H, Manning, A, Mcelligott, S, Mukerji, N, Narayanamurthy, H, O’brien, D, Okasha, M, Papadopoulos, M, Phan, V, Phang, I, Poots, J, Rajaraman, C, Ross, N, Sharouf, F, Shastin, D, Simms, N, Steele, L, Tajsic, T, Talibi, S, Thanabalasundaram, G, Vintu, M, Wan, Y, Wang, D, Watkins, L, Whitehouse, K, Whitfield, PC, and Williams, A

Published
2018
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