ORCID Profile
0000-0003-4902-1462
Current Organisations
Australian Bureau of Meteorology
,
CSIRO
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Atmospheric Dynamics | Atmospheric Sciences | Physical Oceanography | Meteorology | Climate Change Processes
Atmospheric Processes and Dynamics | Climate Variability (excl. Social Impacts) | Climate Change Models |
Publisher: Elsevier BV
Date: 09-2018
Publisher: Springer Science and Business Media LLC
Date: 24-05-2019
Publisher: Springer Science and Business Media LLC
Date: 10-08-2021
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22551388.V1
Abstract: Supplementary Figure S1. The majority of Pb-Cre PTENfl/fl Trp53fl/fl mice are de novo resistant to ADT. Supplementary Figure S2. ADT/PI3Ki combination therapy halts prostate tumor growth up to 14 days, followed by development of resistance in majority of Pb-Cre PTENfl/fl Trp53fl/fl mice. Supplementary Figure S3. PI3Ki treatment with concurrent androgen depletion does not alter proliferation and survival of PTEN 53-deficient murine PC cells in vitro. Supplementary Figure S4. ADT/PI3K inhibitor combination increases MHC-II and PD-1 expression on TAM within the TME of PTEN 53-deficient murine PC. Supplementary Figure S5. PD-1 upregulation suppresses phagocytic capacity of activated TAM. Supplementary Figure S6. Ex vivo AD + PI3Ki + PD-1 antibody treatment activates MHCIIlo TAM when co-cultured with PTEN 53-deficient murine prostate tumor cells. Supplementary Figure S7. The addition of PD-1 blockade to androgen depletion/PI3Ki therapy does not alter phagocytic capacity of PD-1 lo macrophages. Supplementary Figure S8. The combination of androgen depletion, PI3Ki and aPD-1 blockade does not alter phagocytic checkpoint expression on PTEN 53-deficient prostate tumor cells. Supplementary Figure S9. Androgen depletion, singly and in combination with aPD-1, did not alter phagocytosis activity of inactivated MHC-IIlo/PD-1 lo and MHC-IIlo/PD-1 hi TAM subsets. Supplementary Figure S10. Androgen depletion, not PI3Ki or aPD1, directly enhances TAM activation within the TME of PTEN 53-deficient PC. Supplementary Figure S11. PI3Ki does not alter phagocytosis/histone lactylation status of MHC-IIlo/PD-1 lo TAM and MHC-IIlo/PD-1 hi TAM. Supplementary Figure S12. PI3Ki inhibits lactate secretion from PTEN 53-deficient prostate tumor cells within TME. Supplementary Figure S13. Direct ex vivo treatment of TAM with PI3Ki, singly and in combination with PD-1 antibody and/or androgen depletion does not alter their histone lactylation profile. Supplementary Figure S14. ADT + PI3Ki + aPD-1 induces tumor control in 60% of Pb-Cre PTENfl/fl TP53fl/fl mice. Supplementary Figure S15. Depletion of activated TAM abrogates anti-cancer response elicited by ADT + PI3Ki + PD-1 antibody treatment in the PTEN 53-deficient murine prostate GEMM tumors. Supplementary Figure S16. Long-term treatment of ADT + PI3Ki + aPD-1 activates Wnt/βcatenin pathway in murine PTEN 53-deficient GEMM-derived SC1 cells. Supplementary Figure S17. Feedback Wnt/β-catenin-pathway activation within murine PTEN 53-deficient GEMM-derived PC cells following long-term ADT + copanlisib + aPD1 treatment suppresses phagocytosis via increased histone lactylation within bone marrow derived macrophages (BMDM).
Publisher: American Geophysical Union (AGU)
Date: 02-2018
DOI: 10.1002/2017JC013326
Publisher: American Geophysical Union (AGU)
Date: 10-10-2006
DOI: 10.1029/2005JD006860
Publisher: Wiley
Date: 22-10-2023
DOI: 10.1002/QJ.4585
Publisher: American Geophysical Union (AGU)
Date: 03-06-2009
DOI: 10.1029/2008JD010346
Publisher: Springer Science and Business Media LLC
Date: 26-10-2013
Publisher: Springer Science and Business Media LLC
Date: 05-05-2006
Publisher: Elsevier BV
Date: 12-2015
Publisher: American Geophysical Union (AGU)
Date: 19-09-2009
DOI: 10.1029/2009JD011737
Publisher: American Geophysical Union (AGU)
Date: 06-04-2021
DOI: 10.1029/2020GL091131
Abstract: Using an extended 120‐year record of El Niño events, we distinguish between central Pacific (CP) and eastern Pacific (EP) types to show that the strength of CP events is a factor in the litude and sign of the impact on rainfall over southeastern Australia. Both weak and strong CP events cause widespread rainfall deficits in Australia during the onset phase from April to September. However, this relationship reverses over southeastern Australia including the Murray Darling Basin river catchment region for the strongest CP events after October, leading to positive rainfall anomalies during the mature phase of strong CP El Niños. This reversal can be explained by a change in the circulation over eastern Australia from drier, more westerly orientated flow to moister, more easterly onshore flow. These findings may help with seasonal prediction efforts to predict drought‐breaking rain such as occurred in early 2020.
Publisher: American Geophysical Union (AGU)
Date: 19-12-2015
DOI: 10.1002/2015GL067086
Publisher: Springer Science and Business Media LLC
Date: 20-02-2021
Publisher: CSIRO Publishing
Date: 09-12-2022
DOI: 10.1071/ES22026
Abstract: ACCESS-S2 is a major upgrade to the Australian Bureau of Meteorology’s multi-week to seasonal prediction system. It was made operational in October 2021, replacing ACCESS-S1. The focus of the upgrade is the addition of a new weakly coupled data assimilation system to provide initial conditions for atmosphere, ocean, land and ice fields. The model is based on the UK Met Office GloSea5-GC2 seasonal prediction system and is unchanged from ACCESS-S1, aside from minor corrections and enhancements. The performance of the assimilation system and the skill of the seasonal and multi-week forecasts have been assessed and compared to ACCESS-S1. There are improvements in the ACCESS-S2 initial conditions compared to ACCESS-S1, particularly for soil moisture and aspects of the ocean, notably the ocean currents. More realistic soil moisture initialisation has led to increased skill for forecasts over Australia, especially those of maximum temperature. The ACCESS-S2 system is shown to have increased skill of El Nino–Southern Oscillation forecasts over ACCESS-S1 during the challenging autumn forecast period. Analysis suggests that ACCESS-S2 will deliver improved operational forecast accuracy in comparison to ACCESS-S1. Assessments of the operational forecasts are underway. ACCESS-S2 represents another step forward in the development of seasonal forecast systems at the Bureau of Meteorology. However, key rainfall and sea surface temperature biases in ACCESS-S1 remain in ACCESS-S2, indicating where future efforts should be focused.
Publisher: Springer Science and Business Media LLC
Date: 10-12-2010
Publisher: Springer Science and Business Media LLC
Date: 10-12-2013
Publisher: Elsevier
Date: 2016
DOI: 10.1016/BS.AMB.2016.04.002
Abstract: Climate influences marine ecosystems on a range of time scales, from weather-scale (days) through to climate-scale (hundreds of years). Understanding of interannual to decadal climate variability and impacts on marine industries has received less attention. Predictability up to 10 years ahead may come from large-scale climate modes in the ocean that can persist over these time scales. In Australia the key drivers of climate variability affecting the marine environment are the Southern Annular Mode, the Indian Ocean Dipole, the El Niño/Southern Oscillation, and the Interdecadal Pacific Oscillation, each has phases that are associated with different ocean circulation patterns and regional environmental variables. The roles of these drivers are illustrated with three case studies of extreme events-a marine heatwave in Western Australia, a coral bleaching of the Great Barrier Reef, and flooding in Queensland. Statistical and dynamical approaches are described to generate forecasts of climate drivers that can subsequently be translated to useful information for marine end users making decisions at these time scales. Considerable investment is still needed to support decadal forecasting including improvement of ocean-atmosphere models, enhancement of observing systems on all scales to support initiation of forecasting models, collection of important biological data, and integration of forecasts into decision support tools. Collaboration between forecast developers and marine resource sectors-fisheries, aquaculture, tourism, bio ersity management, infrastructure-is needed to support forecast-based tactical and strategic decisions that reduce environmental risk over annual to decadal time scales.
Publisher: American Geophysical Union (AGU)
Date: 05-01-2015
DOI: 10.1002/2014GL062509
Publisher: Springer Science and Business Media LLC
Date: 20-11-2022
Publisher: American Geophysical Union (AGU)
Date: 25-08-2010
DOI: 10.1029/2009JD012643
Publisher: American Meteorological Society
Date: 06-2016
Abstract: There has been increasing demand in Australia for extended-range forecasts of extreme heat events. An assessment is made of the subseasonal experimental guidance provided by the Bureau of Meteorology’s seasonal prediction system, Predictive Ocean Atmosphere Model for Australia (POAMA, version 2), for the three most extreme heat events over Australia in 2013, which occurred in January, March, and September. The impacts of these events included devastating bushfires and damage to crops. The outlooks performed well for January and September, with forecasts indicating increased odds of top-decile maximum temperature over most affected areas at least one week in advance for the fortnightly averaged periods at the start of the heat waves and for forecasts of the months of January and September. The March event was more localized, affecting southern Australia. Although the anomalously high sea surface temperature around southern Australia in March (a potential source of predictability) was correctly forecast, the forecast of high temperatures over the mainland was restricted to the coastline. September was associated with strong forcing from some large-scale atmospheric climate drivers known to increase the chance of having more extreme temperatures over parts of Australia. POAMA-2 was able to forecast the sense of these drivers at least one week in advance, but their magnitude was weaker than observed. The reasonably good temperature forecasts for September are likely due to the model being able to forecast the important climate drivers and their teleconnection to Australian climate. This study adds to the growing evidence that there is significant potential to extend and augment traditional weather forecast guidance for extreme events to include longer-lead probabilistic information.
Publisher: American Meteorological Society
Date: 12-2009
Abstract: The impact of explosive volcanic eruptions on the atmospheric circulation at high northern latitudes is assessed in two versions of the Met Office Hadley Centre’s atmospheric climate model. The standard version of the model extends to an altitude of around 40 km, while the extended version has enhanced stratospheric resolution and reaches 85-km altitude. Seasonal hindcasts initialized on 1 December produce a strengthening of the winter polar vortex and anomalous warming over northern Europe characteristic of the positive phase of the Arctic Oscillation (AO) when forced with volcanic aerosol following the 1963 Mount Agung, 1982 El Chichón, and 1991 Mount Pinatubo eruptions, as is observed. The AO signal in the extended model is of comparable strength to that in the standard model, showing that there is little impact from both increasing the vertical resolution in the stratosphere and extending the model domain to near the mesopause. The presence of this signal in the models, however, is likely due to the persistence of the observed signal from the initial conditions, because a similar set of experiments initiated with the same conditions, but with no volcanic aerosol forcing, exhibits a similar response as the forced runs. This suggests that the model has limited fidelity in capturing the response to volcanic aerosols on its own, consistent with previous studies on the impact of volcanic forcing in long climate simulations, but does support the premise that seasonal winter forecasts are substantially improved with the inclusion of stratospheric information.
Publisher: Springer Science and Business Media LLC
Date: 09-01-2014
Publisher: Cold Spring Harbor Laboratory
Date: 03-06-2019
DOI: 10.1101/657676
Abstract: As more datasets, tools, workflows, APIs, and other digital resources are produced by the research community, it is becoming increasingly difficult to harmonize and organize these efforts for maximal synergistic integrated utilization. The Findable, Accessible, Interoperable, and Reusable (FAIR) guiding principles have prompted many stakeholders to consider strategies for tackling this challenge by making these digital resources follow common standards and best practices so that they can become more integrated and organized. Faced with the question of how to make digital resources more FAIR, it has become imperative to measure what it means to be FAIR. The ersity of resources, communities, and stakeholders have different goals and use cases and this makes assessment of FAIRness particularly challenging. To begin resolving this challenge, the FAIRshake toolkit was developed to enable the establishment of community-driven FAIR metrics and rubrics paired with manual, semi- and fully-automated FAIR assessment capabilities. The FAIRshake toolkit contains a database that lists registered digital resources, with their associated metrics, rubrics, and assessments. The FAIRshake toolkit also has a browser extension and a bookmarklet that enables viewing and submitting assessments from any website. The FAIR assessment results are visualized as an insignia that can be viewed on the FAIRshake website, or embedded within hosting websites. Using FAIRshake, a variety of bioinformatics tools, datasets listed on dbGaP, APIs registered in SmartAPI, workflows in Dockstore, and other biomedical digital resources were manually and automatically assessed for FAIRness. In each case, the assessments revealed room for improvement, which prompted enhancements that significantly upgraded FAIRness scores of several digital resources.
Publisher: Springer Science and Business Media LLC
Date: 12-10-2017
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820230.V1
Abstract: Supplementary Figure S1. The majority of Pb-Cre PTENfl/fl Trp53fl/fl mice are de novo resistant to ADT.Supplementary Figure S2. ADT/PI3Ki combination therapy halts prostate tumor growth up to 14 days, followed by development of resistance in majority of Pb-Cre PTENfl/fl Trp53fl/fl mice.Supplementary Figure S3. PI3Ki treatment with concurrent androgen depletion does not alter proliferation and survival of PTEN 53-deficient murine PC cells in vitro.Supplementary Figure S4. ADT/PI3K inhibitor combination increases MHC-II and PD-1 expression on TAM within the TME of PTEN 53-deficient murine PC.Supplementary Figure S5. PD-1 upregulation suppresses phagocytic capacity of activated TAM.Supplementary Figure S6. Ex vivo AD + PI3Ki + PD-1 antibody treatment activates MHCIIlo TAM when co-cultured with PTEN 53-deficient murine prostate tumor cells.Supplementary Figure S7. The addition of PD-1 blockade to androgen depletion/PI3Ki therapy does not alter phagocytic capacity of PD-1 lo macrophages.Supplementary Figure S8. The combination of androgen depletion, PI3Ki and aPD-1 blockade does not alter phagocytic checkpoint expression on PTEN 53-deficient prostate tumor cells.Supplementary Figure S9. Androgen depletion, singly and in combination with aPD-1, did not alter phagocytosis activity of inactivated MHC-IIlo/PD-1 lo and MHC-IIlo/PD-1 hi TAM subsets.Supplementary Figure S10. Androgen depletion, not PI3Ki or aPD1, directly enhances TAM activation within the TME of PTEN 53-deficient PC.Supplementary Figure S11. PI3Ki does not alter phagocytosis/histone lactylation status of MHC-IIlo/PD-1 lo TAM and MHC-IIlo/PD-1 hi TAM.Supplementary Figure S12. PI3Ki inhibits lactate secretion from PTEN 53-deficient prostate tumor cells within TME.Supplementary Figure S13. Direct ex vivo treatment of TAM with PI3Ki, singly and in combination with PD-1 antibody and/or androgen depletion does not alter their histone lactylation profile.Supplementary Figure S14. ADT + PI3Ki + aPD-1 induces tumor control in 60% of Pb-Cre PTENfl/fl TP53fl/fl mice.Supplementary Figure S15. Depletion of activated TAM abrogates anti-cancer response elicited by ADT + PI3Ki + PD-1 antibody treatment in the PTEN 53-deficient murine prostate GEMM tumors.Supplementary Figure S16. Long-term treatment of ADT + PI3Ki + aPD-1 activates Wnt/βcatenin pathway in murine PTEN 53-deficient GEMM-derived SC1 cells.Supplementary Figure S17. Feedback Wnt/β-catenin-pathway activation within murine PTEN 53-deficient GEMM-derived PC cells following long-term ADT + copanlisib + aPD1 treatment suppresses phagocytosis via increased histone lactylation within bone marrow derived macrophages (BMDM).
Publisher: American Meteorological Society
Date: 25-11-2013
Abstract: The seasonal cycle of blocking in the Australian region is shown to be associated with major seasonal temperature changes over continental Antarctica (approximately 15°–35°C) and Australia (about 8°–17°C) and with minor changes over the surrounding oceans (below 5°C). These changes are superimposed on a favorable background state for blocking in the region resulting from a conjunction of physical influences. These include the geographical configuration and topography of the Australian and Antarctic continents and the positive west to east gradient of sea surface temperature in the Indo-Australian sector of the Southern Ocean. Blocking is represented by a blocking index (BI) developed by the Australian Bureau of Meteorology. The BI has a marked seasonal cycle that reflects seasonal changes in the strength of the westerly winds in the midtroposphere at selected latitudes. Significant correlations between the BI at Australian longitudes and rainfall have been demonstrated in southern and central Australia for the austral autumn, winter, and spring. Patchy positive correlations are evident in the south during summer but significant negative correlations are apparent in the central tropical north. By decomposing the rainfall into its contributions from identifiable synoptic types during the April–October growing season, it is shown that the high correlation between blocking and rainfall in southern Australia is explained by the component of rainfall associated with cutoff lows. These systems form the cyclonic components of blocking dipoles. In contrast, there is no significant correlation between the BI and rainfall from Southern Ocean fronts.
Publisher: American Geophysical Union (AGU)
Date: 05-06-2008
DOI: 10.1029/2007JD008981
Publisher: American Geophysical Union (AGU)
Date: 22-01-2020
DOI: 10.1029/2019JD030923
Publisher: American Meteorological Society
Date: 03-2008
Abstract: Simulations using an atmospheric model forced with observed SST climatology and the same atmospheric model coupled to a slab-ocean model are used to investigate the role of air–sea interaction on the dynamics of the MJO. Slab-ocean coupling improved the MJO in Australia’s Bureau of Meteorology atmospheric model over the Indo-Pacific warm pool by reducing its period from 70–100 to 45–70 days, thereby showing better agreement with the 30–80-day observed oscillation. Air–sea coupling improves the MJO by increasing the moisture flux in the lower troposphere prior to the passage of active convection, which acts to promote convection and precipitation on the eastern flank of the main convective center. This process is triggered by an increase in surface evaporation over positive SST anomalies ahead of the MJO convection, which are driven by the enhanced shortwave radiation in the region of suppressed convection. This in turn generates enhanced convergence into the region, which supports evaporation–wind feedback in the presence of weak background westerly winds. A subsequent increase in low-level moisture convergence acts to further moisten the lower troposphere in advance of large-scale convection in a region of reduced atmospheric pressure. This destabilizing mechanism is referred to as enhanced moisture convergence–evaporation feedback (EMCEF) and is utilized to understand the role of air–sea coupling on the observed MJO. The EMCEF mechanism also reconciles traditionally opposing ideas on the roles of frictional wave–conditional instability of the second kind (CISK) and wind–evaporation feedback. These results support the idea that the MJO is primarily an atmospheric phenomenon, with air–sea interaction improving upon, but not critical for, its existence in the model.
Publisher: American Geophysical Union (AGU)
Date: 22-01-2020
DOI: 10.1029/2019JD030920
Publisher: Springer Science and Business Media LLC
Date: 19-03-2019
Publisher: American Geophysical Union (AGU)
Date: 08-2020
DOI: 10.1029/2020JC016354
Publisher: Springer Science and Business Media LLC
Date: 22-01-2015
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820230
Abstract: Supplementary Figure S1. The majority of Pb-Cre PTENfl/fl Trp53fl/fl mice are de novo resistant to ADT.Supplementary Figure S2. ADT/PI3Ki combination therapy halts prostate tumor growth up to 14 days, followed by development of resistance in majority of Pb-Cre PTENfl/fl Trp53fl/fl mice.Supplementary Figure S3. PI3Ki treatment with concurrent androgen depletion does not alter proliferation and survival of PTEN 53-deficient murine PC cells in vitro.Supplementary Figure S4. ADT/PI3K inhibitor combination increases MHC-II and PD-1 expression on TAM within the TME of PTEN 53-deficient murine PC.Supplementary Figure S5. PD-1 upregulation suppresses phagocytic capacity of activated TAM.Supplementary Figure S6. Ex vivo AD + PI3Ki + PD-1 antibody treatment activates MHCIIlo TAM when co-cultured with PTEN 53-deficient murine prostate tumor cells.Supplementary Figure S7. The addition of PD-1 blockade to androgen depletion/PI3Ki therapy does not alter phagocytic capacity of PD-1 lo macrophages.Supplementary Figure S8. The combination of androgen depletion, PI3Ki and aPD-1 blockade does not alter phagocytic checkpoint expression on PTEN 53-deficient prostate tumor cells.Supplementary Figure S9. Androgen depletion, singly and in combination with aPD-1, did not alter phagocytosis activity of inactivated MHC-IIlo/PD-1 lo and MHC-IIlo/PD-1 hi TAM subsets.Supplementary Figure S10. Androgen depletion, not PI3Ki or aPD1, directly enhances TAM activation within the TME of PTEN 53-deficient PC.Supplementary Figure S11. PI3Ki does not alter phagocytosis/histone lactylation status of MHC-IIlo/PD-1 lo TAM and MHC-IIlo/PD-1 hi TAM.Supplementary Figure S12. PI3Ki inhibits lactate secretion from PTEN 53-deficient prostate tumor cells within TME.Supplementary Figure S13. Direct ex vivo treatment of TAM with PI3Ki, singly and in combination with PD-1 antibody and/or androgen depletion does not alter their histone lactylation profile.Supplementary Figure S14. ADT + PI3Ki + aPD-1 induces tumor control in 60% of Pb-Cre PTENfl/fl TP53fl/fl mice.Supplementary Figure S15. Depletion of activated TAM abrogates anti-cancer response elicited by ADT + PI3Ki + PD-1 antibody treatment in the PTEN 53-deficient murine prostate GEMM tumors.Supplementary Figure S16. Long-term treatment of ADT + PI3Ki + aPD-1 activates Wnt/βcatenin pathway in murine PTEN 53-deficient GEMM-derived SC1 cells.Supplementary Figure S17. Feedback Wnt/β-catenin-pathway activation within murine PTEN 53-deficient GEMM-derived PC cells following long-term ADT + copanlisib + aPD1 treatment suppresses phagocytosis via increased histone lactylation within bone marrow derived macrophages (BMDM).
Publisher: American Meteorological Society
Date: 25-11-2013
Abstract: The Australian Bureau of Meteorology has recently enhanced its capability to make coupled model forecasts of intraseasonal climate variations. The Predictive Ocean Atmosphere Model for Australia (POAMA, version 2) seasonal prediction forecast system in operations prior to March 2013, designated P2-S, was not designed for intraseasonal forecasting and has deficiencies in this regard. Most notably, the forecasts were only initialized on the 1st and 15th of each month, and the growth of the ensemble spread in the first 30 days of the forecasts was too slow to be useful on intraseasonal time scales. These deficiencies have been addressed in a system upgrade by initializing more often and through enhancements to the ensemble generation. The new ensemble generation scheme is based on a coupled-breeding approach and produces an ensemble of perturbed atmosphere and ocean states for initializing the forecasts. This scheme impacts favorably on the forecast skill of Australian rainfall and temperature compared to P2-S and its predecessor (version 1.5). In POAMA-1.5 the ensemble was produced using time-lagged atmospheric initial conditions but with unperturbed ocean initial conditions. P2-S used an ensemble of perturbed ocean initial conditions but only a single atmospheric initial condition. The improvement in forecast performance using the coupled-breeding approach is primarily reflected in improved reliability in the first month of the forecasts, but there is also higher skill in predicting important drivers of intraseasonal climate variability, namely the Madden–Julian oscillation and southern annular mode. The results illustrate the importance of having an optimal ensemble generation strategy.
Publisher: Springer Science and Business Media LLC
Date: 09-07-2011
Publisher: American Meteorological Society
Date: 2009
Abstract: This paper presents an analysis of Northern Hemisphere climate regime variability for three different time slices, simulated by the Fast Ocean Atmosphere Model (FOAM). The three time slices are composed of present-day conditions, the mid-Holocene, and the Last Glacial Maximum (LGM). Climate regimes have been determined by analyzing the structure of a spherical probability density function in a low-dimensional state space spanned by the three leading empirical orthogonal functions. This study confirms the ability of the FOAM medium-resolution climate model to reproduce low-frequency climate variability in the form of regime-like behavior. Three to four regimes have been detected for each time slice. Compared with present-day conditions, new climate regimes appeared for the LGM. For the mid-Holocene, which had slightly different boundary conditions and external forcings than the present-day simulation, the frequency of occurrence of the regimes was altered while only slight changes were found in the structure of some regimes.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22551385.V1
Abstract: Supplementary Table S1. ADT + PI3Ki + PD-1 antibody leads to TAM activation within TME of PTEN 53-deficient prostate tumors.
Publisher: American Meteorological Society
Date: 15-01-2023
Abstract: We assess seasonally varying impacts of the Madden–Julian oscillation (MJO) on Australian maximum and minimum temperature anomalies and extremes, and their modulation by El Niño–Southern Oscillation (ENSO), for the period June 1974–May 2022. Our composite-based approach uses observed temperatures from the Australian Gridded Climate Data, and 850-hPa wind data from the NCEP–NCAR reanalysis, to show how relationships to temperature and circulation evolve over the eight-phase life cycle of the MJO, which we derive from the real-time multivariate MJO index. The MJO has significant impacts on Australian temperatures and winds in all parts of the country at various times throughout the year, and to varying degrees. Two of the most pronounced impacts are 1) daytime warming across southeastern Australia in MJO phase 3 during spring associated with a strong anomalous anticyclone and 2) nighttime cooling over Queensland in MJO phase 7 during winter associated with anomalous advection of cool dry continental air. La Niña acts to significantly lessen both of these impacts, while El Niño enhances both the phase 3 warming over southern Australia in spring and the phase 7 overnight cooling over southern Queensland in winter. We show how the MJO can combine with El Niño and La Niña to have strong compounding influences, thus highlighting the importance of understanding interactions between multiple modes of climate variability and how they relate to Australian temperatures and extremes.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820227.V1
Abstract: Supplementary Table S1. ADT + PI3Ki + PD-1 antibody leads to TAM activation within TME of PTEN 53-deficient prostate tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.C.6563227.V1
Abstract: AbstractPurpose: Phosphatase and tensin homolog (PTEN) loss of function occurs in approximately 50% of patients with metastatic castrate-resistant prostate cancer (mCRPC), and is associated with poor prognosis and responsiveness to standard-of-care therapies and immune checkpoint inhibitors. While PTEN loss of function hyperactivates PI3K signaling, combinatorial PI3K/AKT pathway and androgen deprivation therapy (ADT) has demonstrated limited anticancer efficacy in clinical trials. Here, we aimed to elucidate mechanism(s) of resistance to ADT/PI3K-AKT axis blockade, and to develop rational combinatorial strategies to effectively treat this molecular subset of mCRPC. Experimental Design: Prostate-specific PTEN 53-deficient genetically engineered mice (GEM) with established 150–200 mm sup /sup tumors, as assessed by ultrasound, were treated with either ADT (degarelix), PI3K inhibitor (copanlisib), or anti–PD-1 antibody (aPD-1), as single agents or their combinations, and tumors were monitored by MRI and harvested for immune, transcriptomic, and proteomic profiling, or i ex vivo /i co-culture studies. Single-cell RNA sequencing on human mCRPC s les was performed using 10X Genomics platform. Results: Coclinical trials in PTEN 53-deficient GEM revealed that recruitment of PD-1–expressing tumor-associated macrophages (TAM) thwarts ADT/PI3Ki combination–induced tumor control. The addition of aPD-1 to ADT/PI3Ki combination led to TAM-dependent approximately 3-fold increase in anticancer responses. Mechanistically, decreased lactate production from PI3Ki-treated tumor cells suppressed histone lactylation within TAM, resulting in their anticancer phagocytic activation, which was augmented by ADT/aPD-1 treatment and abrogated by feedback activation of Wnt/β-catenin pathway. Single-cell RNA-sequencing analysis in mCRPC patient biopsy s les revealed a direct correlation between high glycolytic activity and TAM phagocytosis suppression. Conclusions: Immunometabolic strategies that reverse lactate and PD-1–mediated TAM immunosuppression, in combination with ADT, warrant further investigation in patients with PTEN-deficient mCRPC. /
Publisher: American Meteorological Society
Date: 04-2009
Abstract: The ocean dynamics of the Madden–Julian oscillation (MJO) and its interaction with El Niño–Southern Oscillation (ENSO) are assessed using a flux-corrected coupled model experiment from the Australian Bureau of Meteorology. The model demonstrates the correct oceanic Kelvin wave response to the MJO-related westerly winds in the western Pacific. Although there may be a role for the MJO in influencing the strength of El Niño, its impact is difficult to separate from that of strong heat content preconditioning of ENSO. Hence, the MJO–ENSO relationship is assessed starting from a background state of low heat content anomalies in the western Pacific that are also characteristic of recent observed El Niño events. The model shows a strong relationship between ENSO and the MJO near the peak of El Niño. At this time, the sea surface temperature (SST) anomaly is largest in the central Pacific, and it is difficult to separate cause and effect. Near the onset of El Niño, however, when Pacific Ocean SST anomalies are near zero, an increase in MJO activity is associated with Kelvin wave activity and stronger subsequent ENSO warming. A significant increase in the number of MJO events, rather than the strength of in idual MJO events, leads to stronger eastern Pacific warming the MJO appears not to be responsible for the occurrence of El Niño itself, but, rather, is important for influencing its development thus. This research supports a role for downwelling oceanic Kelvin waves and subsequent deepening of the thermocline in contributing to eastern Pacific warming during the onset of El Niño.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.C.6563227.V2
Abstract: AbstractPurpose: Phosphatase and tensin homolog (PTEN) loss of function occurs in approximately 50% of patients with metastatic castrate-resistant prostate cancer (mCRPC), and is associated with poor prognosis and responsiveness to standard-of-care therapies and immune checkpoint inhibitors. While PTEN loss of function hyperactivates PI3K signaling, combinatorial PI3K/AKT pathway and androgen deprivation therapy (ADT) has demonstrated limited anticancer efficacy in clinical trials. Here, we aimed to elucidate mechanism(s) of resistance to ADT/PI3K-AKT axis blockade, and to develop rational combinatorial strategies to effectively treat this molecular subset of mCRPC. Experimental Design: Prostate-specific PTEN 53-deficient genetically engineered mice (GEM) with established 150–200 mm sup /sup tumors, as assessed by ultrasound, were treated with either ADT (degarelix), PI3K inhibitor (copanlisib), or anti–PD-1 antibody (aPD-1), as single agents or their combinations, and tumors were monitored by MRI and harvested for immune, transcriptomic, and proteomic profiling, or i ex vivo /i co-culture studies. Single-cell RNA sequencing on human mCRPC s les was performed using 10X Genomics platform. Results: Coclinical trials in PTEN 53-deficient GEM revealed that recruitment of PD-1–expressing tumor-associated macrophages (TAM) thwarts ADT/PI3Ki combination–induced tumor control. The addition of aPD-1 to ADT/PI3Ki combination led to TAM-dependent approximately 3-fold increase in anticancer responses. Mechanistically, decreased lactate production from PI3Ki-treated tumor cells suppressed histone lactylation within TAM, resulting in their anticancer phagocytic activation, which was augmented by ADT/aPD-1 treatment and abrogated by feedback activation of Wnt/β-catenin pathway. Single-cell RNA-sequencing analysis in mCRPC patient biopsy s les revealed a direct correlation between high glycolytic activity and TAM phagocytosis suppression. Conclusions: Immunometabolic strategies that reverse lactate and PD-1–mediated TAM immunosuppression, in combination with ADT, warrant further investigation in patients with PTEN-deficient mCRPC. /
Publisher: Springer Science and Business Media LLC
Date: 28-11-2019
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22551388
Abstract: Supplementary Figure S1. The majority of Pb-Cre PTENfl/fl Trp53fl/fl mice are de novo resistant to ADT. Supplementary Figure S2. ADT/PI3Ki combination therapy halts prostate tumor growth up to 14 days, followed by development of resistance in majority of Pb-Cre PTENfl/fl Trp53fl/fl mice. Supplementary Figure S3. PI3Ki treatment with concurrent androgen depletion does not alter proliferation and survival of PTEN 53-deficient murine PC cells in vitro. Supplementary Figure S4. ADT/PI3K inhibitor combination increases MHC-II and PD-1 expression on TAM within the TME of PTEN 53-deficient murine PC. Supplementary Figure S5. PD-1 upregulation suppresses phagocytic capacity of activated TAM. Supplementary Figure S6. Ex vivo AD + PI3Ki + PD-1 antibody treatment activates MHCIIlo TAM when co-cultured with PTEN 53-deficient murine prostate tumor cells. Supplementary Figure S7. The addition of PD-1 blockade to androgen depletion/PI3Ki therapy does not alter phagocytic capacity of PD-1 lo macrophages. Supplementary Figure S8. The combination of androgen depletion, PI3Ki and aPD-1 blockade does not alter phagocytic checkpoint expression on PTEN 53-deficient prostate tumor cells. Supplementary Figure S9. Androgen depletion, singly and in combination with aPD-1, did not alter phagocytosis activity of inactivated MHC-IIlo/PD-1 lo and MHC-IIlo/PD-1 hi TAM subsets. Supplementary Figure S10. Androgen depletion, not PI3Ki or aPD1, directly enhances TAM activation within the TME of PTEN 53-deficient PC. Supplementary Figure S11. PI3Ki does not alter phagocytosis/histone lactylation status of MHC-IIlo/PD-1 lo TAM and MHC-IIlo/PD-1 hi TAM. Supplementary Figure S12. PI3Ki inhibits lactate secretion from PTEN 53-deficient prostate tumor cells within TME. Supplementary Figure S13. Direct ex vivo treatment of TAM with PI3Ki, singly and in combination with PD-1 antibody and/or androgen depletion does not alter their histone lactylation profile. Supplementary Figure S14. ADT + PI3Ki + aPD-1 induces tumor control in 60% of Pb-Cre PTENfl/fl TP53fl/fl mice. Supplementary Figure S15. Depletion of activated TAM abrogates anti-cancer response elicited by ADT + PI3Ki + PD-1 antibody treatment in the PTEN 53-deficient murine prostate GEMM tumors. Supplementary Figure S16. Long-term treatment of ADT + PI3Ki + aPD-1 activates Wnt/βcatenin pathway in murine PTEN 53-deficient GEMM-derived SC1 cells. Supplementary Figure S17. Feedback Wnt/β-catenin-pathway activation within murine PTEN 53-deficient GEMM-derived PC cells following long-term ADT + copanlisib + aPD1 treatment suppresses phagocytosis via increased histone lactylation within bone marrow derived macrophages (BMDM).
Publisher: American Geophysical Union (AGU)
Date: 27-03-2010
DOI: 10.1029/2009JD012742
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22551385
Abstract: Supplementary Table S1. ADT + PI3Ki + PD-1 antibody leads to TAM activation within TME of PTEN 53-deficient prostate tumors.
Publisher: Annual Reviews
Date: 05-2007
DOI: 10.1146/ANNUREV.EARTH.35.092006.145055
Abstract: Burning has been a near-continuous feature of the Australian environment but has become progressively more important since the mid-Tertiary, associated with the development of the characteristic sclerophyll vegetation. In the Quaternary, the extent of burning has varied temporally and regionally with glacial-interglacial cyclicity. Burning during glacial periods was reduced in drier areas, presumably because of a critical reduction in fuel availability, but increased in relatively wetter areas where fuel levels were high. On both glacial and Holocene timescales, peaks in charcoal often accompany transitions between fire-insensitive vegetation types, suggesting that burning is facilitated during periods of climate change and environmental instability. This suggestion has been supported by the demonstration of close relationships between fire and El Niño activity. Burning has also increased progressively over the past few hundred thousand years with major accelerations around the time of first human settlement of the continent and with the arrival of Europeans. To provide a firmer base for application of paleofire records to environmental management, there is an urgent need for a spatially more-substantial coverage of high-resolution fire records with good chronological control.
Publisher: American Geophysical Union (AGU)
Date: 13-01-2016
DOI: 10.1002/2015GL066984
Publisher: Wiley
Date: 07-2018
DOI: 10.1002/QJ.3260
Publisher: Wiley
Date: 27-09-2006
DOI: 10.1002/JQS.1063
Publisher: Wiley
Date: 21-03-2011
DOI: 10.1002/QJ.769
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820227
Abstract: Supplementary Table S1. ADT + PI3Ki + PD-1 antibody leads to TAM activation within TME of PTEN 53-deficient prostate tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.CCR-22-3350
Abstract: Phosphatase and tensin homolog (PTEN) loss of function occurs in approximately 50% of patients with metastatic castrate-resistant prostate cancer (mCRPC), and is associated with poor prognosis and responsiveness to standard-of-care therapies and immune checkpoint inhibitors. While PTEN loss of function hyperactivates PI3K signaling, combinatorial PI3K/AKT pathway and androgen deprivation therapy (ADT) has demonstrated limited anticancer efficacy in clinical trials. Here, we aimed to elucidate mechanism(s) of resistance to ADT/PI3K-AKT axis blockade, and to develop rational combinatorial strategies to effectively treat this molecular subset of mCRPC. Prostate-specific PTEN 53-deficient genetically engineered mice (GEM) with established 150–200 mm3 tumors, as assessed by ultrasound, were treated with either ADT (degarelix), PI3K inhibitor (copanlisib), or anti–PD-1 antibody (aPD-1), as single agents or their combinations, and tumors were monitored by MRI and harvested for immune, transcriptomic, and proteomic profiling, or ex vivo co-culture studies. Single-cell RNA sequencing on human mCRPC s les was performed using 10X Genomics platform. Coclinical trials in PTEN 53-deficient GEM revealed that recruitment of PD-1–expressing tumor-associated macrophages (TAM) thwarts ADT/PI3Ki combination–induced tumor control. The addition of aPD-1 to ADT/PI3Ki combination led to TAM-dependent approximately 3-fold increase in anticancer responses. Mechanistically, decreased lactate production from PI3Ki-treated tumor cells suppressed histone lactylation within TAM, resulting in their anticancer phagocytic activation, which was augmented by ADT/aPD-1 treatment and abrogated by feedback activation of Wnt/β-catenin pathway. Single-cell RNA-sequencing analysis in mCRPC patient biopsy s les revealed a direct correlation between high glycolytic activity and TAM phagocytosis suppression. Immunometabolic strategies that reverse lactate and PD-1–mediated TAM immunosuppression, in combination with ADT, warrant further investigation in patients with PTEN-deficient mCRPC.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.C.6563227
Abstract: AbstractPurpose: Phosphatase and tensin homolog (PTEN) loss of function occurs in approximately 50% of patients with metastatic castrate-resistant prostate cancer (mCRPC), and is associated with poor prognosis and responsiveness to standard-of-care therapies and immune checkpoint inhibitors. While PTEN loss of function hyperactivates PI3K signaling, combinatorial PI3K/AKT pathway and androgen deprivation therapy (ADT) has demonstrated limited anticancer efficacy in clinical trials. Here, we aimed to elucidate mechanism(s) of resistance to ADT/PI3K-AKT axis blockade, and to develop rational combinatorial strategies to effectively treat this molecular subset of mCRPC. Experimental Design: Prostate-specific PTEN 53-deficient genetically engineered mice (GEM) with established 150–200 mm sup /sup tumors, as assessed by ultrasound, were treated with either ADT (degarelix), PI3K inhibitor (copanlisib), or anti–PD-1 antibody (aPD-1), as single agents or their combinations, and tumors were monitored by MRI and harvested for immune, transcriptomic, and proteomic profiling, or i ex vivo /i co-culture studies. Single-cell RNA sequencing on human mCRPC s les was performed using 10X Genomics platform. Results: Coclinical trials in PTEN 53-deficient GEM revealed that recruitment of PD-1–expressing tumor-associated macrophages (TAM) thwarts ADT/PI3Ki combination–induced tumor control. The addition of aPD-1 to ADT/PI3Ki combination led to TAM-dependent approximately 3-fold increase in anticancer responses. Mechanistically, decreased lactate production from PI3Ki-treated tumor cells suppressed histone lactylation within TAM, resulting in their anticancer phagocytic activation, which was augmented by ADT/aPD-1 treatment and abrogated by feedback activation of Wnt/β-catenin pathway. Single-cell RNA-sequencing analysis in mCRPC patient biopsy s les revealed a direct correlation between high glycolytic activity and TAM phagocytosis suppression. Conclusions: Immunometabolic strategies that reverse lactate and PD-1–mediated TAM immunosuppression, in combination with ADT, warrant further investigation in patients with PTEN-deficient mCRPC. /
Publisher: American Geophysical Union (AGU)
Date: 09-2021
DOI: 10.1029/2021JC017591
Abstract: Sea surface temperature (SST) variability in the western half of the Niño 4 region (Niño‐4W), bounded by 160°E−175°W and 5°S–5°N, has a significant impact on weather and the marine environment of the Indo‐Pacific. It exhibits significant negative skewness, with the strong penetration of the cold tongue into the western Pacific during strong La Niñas but a more muted response during El Niños. Zonal advection plays a dominant role in driving Niño‐4W SST cooling during the strong La Niña events vertical processes also contribute, with air‐sea heat fluxes providing weak negative feedback. Advection also plays a key role in driving the Niño‐4W SST warming, which is not always in sync with El Niño events. Among the advection terms, the advection of mean temperature by zonal velocity anomalies, or zonal advective feedback, plays a key role during the development phase of the warm and cold events. Strong negative air‐sea heat flux anomalies during the development of warm events are linked to the negative SST skewness in the Niño‐4W region.
Publisher: Springer Science and Business Media LLC
Date: 09-08-2022
DOI: 10.1038/S41467-022-32205-3
Abstract: There are only a few platforms that integrate multiple omics data types, bioinformatics tools, and interfaces for integrative analyses and visualization that do not require programming skills. Here we present iLINCS ( ilincs.org ), an integrative web-based platform for analysis of omics data and signatures of cellular perturbations. The platform facilitates mining and re-analysis of the large collection of omics datasets ( ,000), pre-computed signatures ( ,000), and their connections, as well as the analysis of user-submitted omics signatures of diseases and cellular perturbations. iLINCS analysis workflows integrate vast omics data resources and a range of analytics and interactive visualization tools into a comprehensive platform for analysis of omics signatures. iLINCS user-friendly interfaces enable execution of sophisticated analyses of omics signatures, mechanism of action analysis, and signature-driven drug repositioning. We illustrate the utility of iLINCS with three use cases involving analysis of cancer proteogenomic signatures, COVID 19 transcriptomic signatures and mTOR signaling.
Publisher: American Geophysical Union (AGU)
Date: 14-12-2016
DOI: 10.1002/2016GL071423
Publisher: CSIRO Publishing
Date: 16-07-2021
DOI: 10.1071/ES21001
Abstract: We assessed the ability of the Bureau of Meteorology’s ACCESS-S1 dynamical forecast system to simulate and predict high rainfall extremes for each season over Australia, especially focusing on the role of the Madden-Julian Oscillation (MJO). Using retrospective forecasts for the period 1990–2012, we show that ACCESS-S1 simulated the observed modulation of extreme weekly mean rainfall by each phase of the MJO reasonably well however the simulated changes in probabilities tended to be weaker than those observed, especially across the far north during the austral summer season. The ability of the model to (i) simulate the observed modulation of extreme rainfall and (ii) predict the MJO to a lead time of four weeks, translated to enhanced forecast skill for predicting the occurrence of extreme weekly mean rainfall across much of Australia at times when the MJO was strong, compared to when the MJO was weak, during the austral spring and summer seasons in weeks 2 and 3. However, skill reduced across the central far north during the summer when the MJO was strong, suggesting the model is not good at depicting the MJO’s convective phases as it protrudes southward over northern Australia. During autumn and winter, there was little indication of changes in forecast skill, depending on the strength of the MJO. The results of this study will be useful for regional applications when the MJO is forecast to be strong during spring and summer, particularly where the swing in probability of extreme rainfall is large for specific phases of the MJO.
Location: Australia
Location: United Kingdom of Great Britain and Northern Ireland
Start Date: 08-2017
End Date: 12-2024
Amount: $30,050,000.00
Funder: Australian Research Council
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