164 research outputs found

    Assessment of CO2 storage capacity and injectivity in saline aquifers – comparison of results from numerical flow simulations, analytical and generic models

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    AbstractMethodologies for the basin-scale evaluation of industrial-scale CO2 geological storage in saline aquifers can include the use of analytical tools, generic reservoir simulations, as well as basin-specific flow modelling studies. The selection of appropriate tools is dependent on the scale of investigation. Comparison of the results from these methods for the assessment of basin-scale CO2 geological storage in the Gippsland and Otway basins in Australia suggests that, at this scale, a combination of analytical tools in the form of equations for calculating injection pressure, radius of impact and storage capacity with generic numerical simulations may provide useful first-order predictions for storage capacity and injectivity. However, the development of multiple resources (petroleum, groundwater, coal) in the Gippsland Basin and regional compartmentalisation in the Otway Basin necessitates an additional, coarsely discretised basin-scale numerical model

    Fisheries and Aquaculture Production in Reservoirs in Lao PDR

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    MK19 Fisheries and Aquaculture Production in Reservoirs in Lao PDRThe project’s overall aim is to provide better information on reservoir fisheries and aquaculture so that reservoirs will be planned and managed to provide a broader range of benefits, particularly to rural people living nearby. Some specific questions which the project is addressing include the following

    Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy.

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    Using a standard confocal setup, a UV ablation method can be utilized to selectively induce cellular injury and to visualize single-cell responses and cell-cell interactions in the CNS in real-time. Previously, studying these cell-specific responses after injury often required complicated setups or the transfer of cells or animals into different, non-physiological environments, confounding immediate and short-term analysis. For example, drug-mediated ablation approaches often lack the specificity that is required to study single-cell responses and immediate cell-cell interactions. Similarly, while high-power pulsed laser ablation approaches provide very good control and tissue penetration, they require specialized equipment that can complicate real-time visualization of cellular responses. The refined UV laser ablation approach described here allows researchers to stress or kill an individual cell in a dose- and time-dependent manner using a conventional confocal microscope equipped with a 405-nm laser. The method was applied to selectively ablate a single neuron within a dense network of surrounding cells in the zebrafish spinal cord. This approach revealed a dose-dependent response of the ablated neurons, causing the fragmentation of cellular bodies and anterograde degeneration along the axon within minutes to hours. This method allows researchers to study the fate of an individual dying cell and, importantly, the instant response of cells-such as microglia and astrocytes-surrounding the ablation site

    KCC1 Activation protects Mice from the Development of Experimental Cerebral Malaria.

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    Plasmodium falciparum malaria causes half a million deaths per year, with up to 9% of this mortality caused by cerebral malaria (CM). One of the major processes contributing to the development of CM is an excess of host inflammatory cytokines. Recently K+ signaling has emerged as an important mediator of the inflammatory response to infection; we therefore investigated whether mice carrying an ENU induced activation of the electroneutral K+ channel KCC1 had an altered response to Plasmodium berghei. Here we show that Kcc1M935K/M935K mice are protected from the development of experimental cerebral malaria, and that this protection is associated with an increased CD4+ and TNFa response. This is the first description of a K+ channel affecting the development of experimental cerebral malaria

    Bone marrow transplantation corrects haemolytic anaemia in a novel ENU mutagenesis mouse model of TPI deficiency.

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    In this study, we performed a genome-wide N-ethyl-N-nitrosourea (ENU) mutagenesis screen in mice to identify novel genes or alleles that regulate erythropoiesis. Here, we describe a recessive mouse strain, called RBC19, harbouring a point mutation within the housekeeping gene, Tpi1, which encodes the glycolysis enzyme, triosephosphate isomerase (TPI). A serine in place of a phenylalanine at amino acid 57 severely diminishes enzyme activity in red blood cells and other tissues, resulting in a macrocytic haemolytic phenotype in homozygous mice, which closely resembles human TPI deficiency. A rescue study was performed using bone marrow transplantation of wild-type donor cells, which restored all haematological parameters and increased red blood cell enzyme function to wild-type levels after 7 weeks. This is the first study performed in a mammalian model of TPI deficiency, demonstrating that the haematological phenotype can be rescued

    OXSR1 inhibits inflammasome activation by limiting potassium efflux during mycobacterial infection.

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    Pathogenic mycobacteria inhibit inflammasome activation to establish infection. Although it is known that potassium efflux is a trigger for inflammasome activation, the interaction between mycobacterial infection, potassium efflux, and inflammasome activation has not been investigated. Here, we use Mycobacterium marinum infection of zebrafish embryos and Mycobacterium tuberculosis infection of THP-1 cells to demonstrate that pathogenic mycobacteria up-regulate the host WNK signalling pathway kinases SPAK and OXSR1 which control intracellular potassium balance. We show that genetic depletion or inhibition of OXSR1 decreases bacterial burden and intracellular potassium levels. The protective effects of OXSR1 depletion are at least partially mediated by NLRP3 inflammasome activation, caspase-mediated release of IL-1β, and downstream activation of protective TNF-α. The elucidation of this druggable pathway to potentiate inflammasome activation provides a new avenue for the development of host-directed therapies against intracellular infections
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