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University of Queensland

University of Queensland

43 Projects, page 1 of 9
  • Funder: UK Research and Innovation Project Code: EP/V029487/1
    Funder Contribution: 6,075 GBP

    In this proposal, I want to develop optimisation frameworks that will use smart card and mobility-as-a-service subscription data to address strategic (transit route network design problem) and (if time allows) tactical (frequency setting and timetabling) public transport planning problems. The use of public transportation is decreasing all around the UK, except London, every year. Last year, more than 80% of the distances are travelled by private cars in Britain. There may be many reasons for the lack of enthusiasm for public transport, e.g. poor connections, infrequent service or high cost. Making public transport again the main mode of transport is important for many reasons. First, the UK's zero carbon emission by 2050 pledge requires to use more energy-efficient modes. More than 16% of the emissions in the UK are from private cars. Second, cars waste road space, they need almost eight times more space per passenger compared to busses. Excessive private car use is one of the biggest reasons for traffic congestion we experience every day. We need to find ways to move mode choice from private to public transport. One way of altering user behaviour from private to public transport could be frameworking mobility as a service (MaaS) and provide packages that could provide different options to users. MaaS is not a new concept and is in use of different forms all around the world. However, these systems either are just a design concept a platform that provides multiple options and unified payment method for any trip to its users or only allows subscription packages that allow users to access mass public transport modes. In this project, in addition to smart card data, I will be able to work with a subscription-based MaaS data that provides mass and personal public transport (e.g. bikesharing, carsharing, ride-hailing, shared ride-hailing, dial-a-ride) to its users together. Intelligent transportation systems (ITP) applications help us monitor and control public transport system. We also use the collected ITP data to analyse and improve those systems. However, the existing classical models are usually not capable of utilising the mass data produced by the ITP systems every day. We need to develop better methods to deal with high precision data. In this proposal, I aim to develop models that will improve public transport planning by using smart card and MaaS subscription data. In my approach, in addition to mass public transit lines, I want to consider personal public transport options in the development of public transport network design and (if time allows) frequency setting and timetabling problems. With the advancement in mobile technologies and trend towards sharing economy, we see more personal public transport modes in cities. They are encouraged by especially the big cities to provide alternative modes of transportation to their dwellers. We see more people use these transport modes every day. Considering all types of public transportation modes in designing transit route networks could provide better public transport plans for limited resources and eventually increase average welfare for the urban dwellers living in these cities.

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  • Funder: UK Research and Innovation Project Code: BB/L027054/1
    Funder Contribution: 27,245 GBP

    Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

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  • Funder: UK Research and Innovation Project Code: NE/H012435/1
    Funder Contribution: 57,572 GBP

    Brigalow forest communities, are dominated by an acacia tree, Acacia harpophylla (brigalow), and once occupied ~8 M ha across the Brigalow Belt region of northeastern Australia in Queensland, but have been reduced to 8% of their former range through clearing for conversion of the land to pasture. Brigalow forests are only found in this region of the world and support a unique flora and fauna which as an ecological community is now listed as endangered under the Australian Environmental Protection and Biodiversity Conservation Act (EPBC). The recovery plan for Brigalow ecological communities identifies lack of knowledge on the ecology of brigalow as a threat to their recovery and recommends that further research on brigalow and how to restore degraded forests should be carried out. In the proposed research, we will advance the knowledge on the ecology of Brigalow. In particular we will provide empirical evidence that will further our understanding of how brigalow respond to habitat disturbance caused by human activities. Specifically, we will compare dispersal by seed (sexual reproduction) and dispersal by root suckering (clonal reproduction) in remnant and disturbed secondary brigalow (regrowth) forests using genetic markers. This is a unique opportunity to find out about the reproductive biology of the species because brigalow only produces seeds very rarely. Such a rare seed recruitment event occurred early in 2008, for the first time in 60 years, and seedlings established in both remnant and regrowth brigalow. We expect to find that the genetic diversity in adults and seedlings of regrowth brigalow is lower than in remnant brigalow because of extensive root suckering in regrowth Brigalow. Indeed, in regrowth, it is expected that dispersal occurs primarily by clonal reproduction because it allows the species to rapidly colonise open land, but it has never actually been assessed. The lack of genetic diversity in regrowth Brigalow may ultimately have detrimental genetic effects for its viability because genetic diversity enables a species to respond and adapt to change in environmental conditions. One way to help maintain genetic diversity in regrowth Brigalow is to design active management strategies that optimize genetic diversity, for instance by removing suckers (thinning). As we will record the spatial location of trees and seedlings, as well as identify their genetic identity, we will be able to produce a geographic map of the location of clones and the distance of dispersal of seeds and we will be able to use this information in a model to predict which thinning management strategy best optimises genetic diversity in restored brigalow stands, as well as restore forest structure and carbon sequestration (which is how much carbon is stored in the trees) to the levels of mature remnant forests. This has economic implications for carbon markets and mined-land rehabilitation.The proposed research will considerably advance our knowledge of the biology of brigalow acacia in its natural environment, and will contribute to fill the gap of knowledge identified by the EPBC on how to successfully restore degraded Brigalow communities. We will make practical recommendations to inform sustainable restoration management of Brigalow forests. Generally, the project will further our understanding of how tree species respond to habitat disturbance, especially for partially clonal species for which no empirical data are available. This is important because degraded regrowth forests are now predominant worldwide, and we need to understand how tree species respond to widespread disturbance as a result of human activities in order to carry out economic activities in an environmentally sustainable way. Finally, this project will present a genetic model of thinning management, which is novel in restoration ecology. The approach, when adopted elsewhere, will improve the long-term sustainability of ecological restoration programmes.

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  • Funder: UK Research and Innovation Project Code: BB/V003607/1
    Funder Contribution: 3,000 GBP

    Australia and New Zealand

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  • Funder: UK Research and Innovation Project Code: BB/R017956/1
    Funder Contribution: 388,116 GBP

    We will develop and test a new intracellular peptide-library screening assay that we have created to derive functional antagonists for a family of transcription factors (bZIP proteins) implicated in disease. Using a cancer causing member that binds DNA, Activator Protein-1 (AP-1), as an exemplar we have recently established a proof-of-principle for our approach. AP-1 is a major player in cancer that functions by binding specific DNA sites to control the expression of genes involved in cellular processes such as cell growth. A major strength of our screening technique is that it selects inhibitors by their ability to bind AP-1, but also ensures they shut down its function. This ability to distinguish between AP-1 binders and those that are capable of shutting down AP-1 function is unique and addresses a problem that has hampered the search for 'functionally active' inhibitors. Since the assay is undertaken entirely inside living bacterial cells, it allows for additional benefits such as removal of library members that do not bind specifically to AP-1, as well as those that are unstable, insoluble, or degraded by enzymes. The project will generate understanding about how AP-1 binds to DNA and how its activity can be prevented, as well as creating peptides with excellent potential to be further developed into druggable molecules. We will test the potency of our peptides and peptide-derived molecules using a range of biophysical, structural, and cell-based experiments, including high-resolution imaging techniques that will allow us to study how our inhibitors work by looking at individual molecules. These experiments will shed light on how our inhibitors work looking for their ability not only to bind to AP-1 but importantly to shut down its function, we will gain an understanding of dosages required, where the inhibitors bind and how quickly, if they are stable in biological fluids, can cross biological membranes, and how they behave in cancer cell cultures where AP-1 is known to play a major role. The importance of these experiments is that we can derive a rule set for the design of inhibitors, enabling us to enhance certain properties of the inhibitors at will. In addition, this rule set can then be applied to rationally design inhibitors for this and other transcription factors.

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