Articles by Elinor Hortle in JoVE
Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy Marco Morsch1, Rowan A. W. Radford1, Emily K. Don1, Albert Lee1, Elinor Hortle1, Nicholas J. Cole1, Roger S. Chung1 1Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University Targeted manipulations to cause directed stress or death in individual cells have been relatively difficult to accomplish. Here, a single-cell-resolution ablation approach to selectively stress and kill individual cells in cell culture and living animals is described based on a standard confocal UV laser.
Other articles by Elinor Hortle on PubMed
Adenosine Monophosphate Deaminase 3 Activation Shortens Erythrocyte Half-life and Provides Malaria Resistance in Mice Blood. Sep, 2016 | Pubmed ID: 27465915 The factors that determine red blood cell (RBC) lifespan and the rate of RBC aging have not been fully elucidated. In several genetic conditions, including sickle cell disease, thalassemia, and G6PD deficiency, erythrocyte lifespan is significantly shortened. Many of these diseases are also associated with protection from severe malaria, suggesting a role for accelerated RBC senescence and clearance in malaria resistance. Here, we report a novel, N-ethyl-N-nitrosourea-induced mutation that causes a gain of function in adenosine 5'-monophosphate deaminase (AMPD3). Mice carrying the mutation exhibit rapid RBC turnover, with increased erythropoiesis, dramatically shortened RBC lifespan, and signs of increased RBC senescence/eryptosis, suggesting a key role for AMPD3 in determining RBC half-life. Mice were also found to be resistant to infection with the rodent malaria Plasmodium chabaudi. We propose that resistance to P. chabaudi is mediated by increased RBC turnover and higher rates of erythropoiesis during infection.
A Tol2 Gateway-Compatible Toolbox for the Study of the Nervous System and Neurodegenerative Disease Zebrafish. Feb, 2017 | Pubmed ID: 27631880 Currently there is a lack in fundamental understanding of disease progression of most neurodegenerative diseases, and, therefore, treatments and preventative measures are limited. Consequently, there is a great need for adaptable, yet robust model systems to both investigate elementary disease mechanisms and discover effective therapeutics. We have generated a Tol2 Gateway-compatible toolbox to study neurodegenerative disorders in zebrafish, which includes promoters for astrocytes, microglia and motor neurons, multiple fluorophores, and compatibility for the introduction of genes of interest or disease-linked genes. This toolbox will advance the rapid and flexible generation of zebrafish models to discover the biology of the nervous system and the disease processes that lead to neurodegeneration.