ORCID Profile
0000-0002-5210-6785
Current Organisations
University of Queensland
,
University of Potsdam
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Publisher: Elsevier BV
Date: 11-2020
Publisher: American Chemical Society (ACS)
Date: 25-11-2019
Publisher: Informa UK Limited
Date: 30-05-2019
DOI: 10.1080/09658211.2019.1623260
Abstract: Although previous research on retrieval practice (RP) has predominantly featured stimuli with discrete right-or-wrong answers, continuous measures offer potentially greater sensitivity in assessing the effects of RP on memory precision. The present study used a colour gradient (125 points ranging from magenta to yellow) as a continuous response variable. The colours of different images were learned through either RP or restudy and either one or three cycles of practice after initial study. On a delayed final test, participants' memory was assessed for each item's colour. Participants also created per-item intervals representing the region where they believed the correct colour most likely to have been. We found that repeated rounds of RP enhanced the correspondence between responses and the correct colour. In addition, RP led to participants creating more accurate (correct answers were more likely to be within the participant-specified intervals) and more precise (narrower) intervals relative to restudy, suggesting that RP enhances the precision of memories.
Publisher: Elsevier BV
Date: 11-2020
Publisher: Elsevier BV
Date: 12-2018
DOI: 10.1016/J.BCP.2018.08.038
Abstract: Recently, we and other groups revealed that gain-of-function mutations in the human ether à go-go voltage-gated potassium channel hEAG1 (K
Publisher: Proceedings of the National Academy of Sciences
Date: 03-08-2018
Abstract: Spider venom is a rich source of peptides, many targeting ion channels. We assessed a venom peptide, Hm1a, as a potential targeted therapy for Dravet syndrome, the genetic epilepsy linked to a mutation in the gene encoding the sodium channel alpha subunit Na V 1.1. Cell-based assays showed Hm1a was selective for hNa V 1.1 over other sodium and potassium channels. Utilizing a mouse model of Dravet syndrome, Hm1a restored inhibitory neuron function and significantly reduced seizures and mortality in heterozygote mice. Evidence from the structure of Hm1a and modeling suggest Hm1a interacts with Na V 1.1 inactivation domains, providing a structural correlate of the functional mechanisms. This proof-of-concept study provides a promising strategy for future drug development in genetic epilepsy and other neurogenetic disorders.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 21-09-2021
DOI: 10.1161/CIRCULATIONAHA.121.054360
Abstract: Ischemia–reperfusion injury (IRI) is one of the major risk factors implicated in morbidity and mortality associated with cardiovascular disease. During cardiac ischemia, the buildup of acidic metabolites results in decreased intracellular and extracellular pH, which can reach as low as 6.0 to 6.5. The resulting tissue acidosis exacerbates ischemic injury and significantly affects cardiac function. We used genetic and pharmacologic methods to investigate the role of acid-sensing ion channel 1a (ASIC1a) in cardiac IRI at the cellular and whole-organ level. Human induced pluripotent stem cell–derived cardiomyocytes as well as ex vivo and in vivo models of IRI were used to test the efficacy of ASIC1a inhibitors as pre- and postconditioning therapeutic agents. Analysis of human complex trait genetics indicates that variants in the ASIC1 genetic locus are significantly associated with cardiac and cerebrovascular ischemic injuries. Using human induced pluripotent stem cell–derived cardiomyocytes in vitro and murine ex vivo heart models, we demonstrate that genetic ablation of ASIC1a improves cardiomyocyte viability after acute IRI. Therapeutic blockade of ASIC1a using specific and potent pharmacologic inhibitors recapitulates this cardioprotective effect. We used an in vivo model of myocardial infarction and 2 models of ex vivo donor heart procurement and storage as clinical models to show that ASIC1a inhibition improves post-IRI cardiac viability. Use of ASIC1a inhibitors as preconditioning or postconditioning agents provided equivalent cardioprotection to benchmark drugs, including the sodium-hydrogen exchange inhibitor zoniporide. At the cellular and whole organ level, we show that acute exposure to ASIC1a inhibitors has no effect on cardiac ion channels regulating baseline electromechanical coupling and physiologic performance. Our data provide compelling evidence for a novel pharmacologic strategy involving ASIC1a blockade as a cardioprotective therapy to improve the viability of hearts subjected to IRI.
Publisher: Society for Learning Analytics Research
Date: 30-08-2023
Abstract: NA
No related grants have been discovered for Brendan Schuetze.