ORCID Profile
0000-0002-5601-7739
Current Organisations
University of Western Australia
,
Ear Science Institute Australia
,
University of Notre Dame Australia
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Publisher: Springer Science and Business Media LLC
Date: 02-01-2019
Publisher: Future Science Ltd
Date: 04-2020
Abstract: Aim: R18D is a poly-arginine peptide that has demonstrated neuroprotection in preclinical models of excitotoxicity, stroke, hypoxic-ischemic encephalopathy and traumatic brain injury. Here, we examined the peptide’s uptake in serum. Materials & methods: Healthy, male Sprague–Dawley rats were intravenously administered either 1000 nmol/kg R18D (D-enantiomer of R18) or approximately 2.5 nmol/kg (36 ± 9 MBq) [ 18 F]R18D, for serum and organ tissue uptake, respectively. Serum s les underwent mass spectrometric analysis to detect unbound R18D peptide. Animals administered [ 18 F]R18D were subjected to positron emission tomography imaging. Results & conclusion: Free R18D was detected at 5 min post-infusion in serum s les. [ 18 F]R18D was rapidly distributed to the kidney (6–7%ID/g), and a small fraction localized to the brain (0.115–0.123%ID/g) over a 60-min acquisition period.
Publisher: Informa UK Limited
Date: 18-02-2016
Publisher: Elsevier BV
Date: 2020
Publisher: Springer Science and Business Media LLC
Date: 14-11-2017
DOI: 10.1007/S12035-016-0287-3
Abstract: Traumatic brain injury (TBI) has a devastating effect on victims and their families, and has profound negative societal and economic impacts, a situation that is further compounded by the lack of effective treatments to minimise injury after TBI. The current strategy for managing TBI is partly through preventative measures and partly through surgical and rehabilitative interventions. Secondary brain damage remains the principal focus for the development of a neuroprotective therapeutic. However, the complexity of TBI pathophysiology has meant that single-action pharmacological agents have been largely unsuccessful in combatting the associated brain injury cascades, while combination therapies to date have proved equally ineffective. Peptides have recently emerged as promising lead agents for the treatment of TBI, especially those rich in the cationic amino acid, arginine. Having been shown to lessen the impact of ischaemic stroke in animal models, there are reasonable grounds to believe that arginine-rich peptides may have neuroprotective therapeutic potential in TBI. Here, we review a range of peptides previously examined as therapeutic agents for TBI. In particular, we focus on cationic arginine-rich peptides -- a new class of agents that growing evidence suggests acts through multiple neuroprotective mechanisms.
Publisher: Walter de Gruyter GmbH
Date: 15-11-2017
Abstract: Cationic arginine-rich and poly-arginine peptides (referred to as CARPs) have potent neuroprotective properties in in vitro excitotoxicity and in vivo models of stroke. Traumatic brain injury (TBI) shares many pathophysiological processes as stroke, including excitotoxicity. Therefore, we evaluated our lead peptide, poly-arginine R18, with the COG1410 and APP96-110 peptides, which have neuroprotective actions following TBI. In an in vitro cortical neuronal glutamic acid excitotoxicity injury model, R18 was highly neuroprotective and reduced neuronal calcium influx, while COG1410 and APP96-110 displayed modest neuroprotection and were less effective at reducing calcium influx. In an impact-acceleration closed-head injury model (Marmarou model), R18, COG1410, and APP96-110 were administered intravenously (300 nmol/kg) at 30 minutes after injury in male Sprague-Dawley rats. When compared to vehicle, no peptide significantly improved functional outcomes, however the R18 and COG1410 treatment groups displayed positive trends in the adhesive tape test and rotarod assessments. Similarly, no peptide had a significant effect on hippoc al neuronal loss, however a significant reduction in axonal injury was observed for R18 and COG1410. In conclusion, this study has demonstrated that R18 is significantly more effective than COG1410 and APP96-110 at reducing neuronal injury and calcium influx following excitotoxicity, and that both R18 and COG1410 reduce axonal injury following TBI. Additional dose response and treatment time course studies are required to further assess the efficacy of R18 in TBI.
Publisher: Sciedu Press
Date: 16-08-2016
No related grants have been discovered for Li Shan Chiu.