Miss Rebecca Hood

Postdoctoral Researcher

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

As a Greaves Family post-graduate scholar, Rebecca's doctoral work focused on understanding the mechanisms underlying the pressure rise within the skull after ischaemic stroke (blockage of an artery in the brain). Since completing her PhD, her postdoctoral career is continuing in the stroke research field with Professor Rohan Walker and Professor Michael Nilsson. Here, her research is focused on post-stroke recovery. 


Qualifications

  • Bachelor of Biomedical Sciences (Hons), University of Newcastle
  • Bachelor of Biomedical Sciences, University of Newcastle

Keywords

  • Biomedical Sciences - Neuroscience
  • Cerebrospinal Fluid
  • Hypoxia
  • Intracranial Pressure
  • Ischaemic Stroke
  • Medical Physiology

Fields of Research

Code Description Percentage
060603 Animal Physiology - Systems 25
060805 Animal Neurobiology 75

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Researcher University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Professional appointment

Dates Title Organisation / Department
1/08/2018 - 4/01/2019 TACTICS VR Project Manager Faculty of Health and Medicine, The University of Newcastle
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (5 outputs)

Year Citation Altmetrics Link
2018 Tan KN, Hood R, Warren K, Pepperall D, Carrasco-Pozo C, Manzanero S, et al., 'Heptanoate is neuroprotective in vitro but triheptanoin post-treatment did not protect against middle cerebral artery occlusion in rats', Neuroscience Letters, 683 207-214 (2018) [C1]

© 2018 Elsevier B.V. Triheptanoin, the medium-chain triglyceride of heptanoate, has been shown to be anticonvulsant and neuroprotective in several neurological disorders. In the g... [more]

© 2018 Elsevier B.V. Triheptanoin, the medium-chain triglyceride of heptanoate, has been shown to be anticonvulsant and neuroprotective in several neurological disorders. In the gastrointestinal tract, triheptanoin is cleaved to heptanoate, which is then taken up by the blood and most tissues, including liver, heart and brain. Here we evaluated the neuroprotective effects of heptanoate and its effects on mitochondrial oxygen consumption in vitro. We also investigated the neuroprotective effects of triheptanoin compared to long-chain triglycerides when administered after stroke onset in rats. Heptanoate pre-treatment protected cultured neurons against cell death induced by oxygen glucose deprivation and N-methyl-D-aspartate. Incubation of cultured astrocytes with heptanoate for 2 h increased mitochondrial proton leak and also enhanced basal respiration and ATP turnover, suggesting that heptanoate protects against oxidative stress and is used as fuel. However, continuous 72 h infusion of triheptanoin initiated 1 h after middle cerebral artery occlusion in rats did not alter stroke volume at 3 days or neurological deficit at 1 and 3 days relative to long-chain triglyceride control treatment.

DOI 10.1016/j.neulet.2018.07.045
Citations Scopus - 1Web of Science - 1
Co-authors Neil Spratt
2016 Beard DJ, Logan CL, McLeod DD, Hood RJ, Pepperall D, Murtha LA, Spratt NJ, 'Ischemic penumbra as a trigger for intracranial pressure rise - A potential cause for collateral failure and infarct progression?', J Cereb Blood Flow Metab, 36 917-927 (2016) [C1]
DOI 10.1177/0271678X15625578
Citations Scopus - 6Web of Science - 3
Co-authors Damian Mcleod, Neil Spratt, Lucy Murtha
2016 Tomkins AJ, Hood RJ, Pepperall D, Null CL, Levi CR, Spratt NJ, 'Thrombolytic Recanalization of Carotid Arteries Is Highly Dependent on Degree of Stenosis, Despite Sonothrombolysis.', J Am Heart Assoc, 5 (2016) [C1]
DOI 10.1161/JAHA.115.002716
Citations Scopus - 2Web of Science - 2
Co-authors Neil Spratt, Christopher Levi
2015 Mcleod DD, Parsons MW, Hood R, Hiles B, Allen J, Mccann SK, et al., 'Perfusion computed tomography thresholds defining ischemic penumbra and infarct core: Studies in a rat stroke model', International Journal of Stroke, 10 553-559 (2015) [C1]

© 2013 World Stroke Organization. Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (isch... [more]

© 2013 World Stroke Organization. Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stroke and guide reperfusion therapies. Aims: The study aims to determine whether there are important changes in perfusion computed tomography thresholds defining ischemic penumbra and infarct core over time following stroke. Methods: Permanent middle cerebral artery occlusion was performed in adult outbred Wistar rats (n=6) and serial perfusion computed tomography scans were taken every 30 mins for 2h. To define infarction thresholds at 1h and 2h post-stroke, separate groups of rats underwent 1h (n=6) and 2h (n=6) of middle cerebral artery occlusion followed by reperfusion. Infarct volumes were defined by histology at 24h. Co-registration with perfusion computed tomography maps (cerebral blood flow, cerebral blood volume, and mean transit time) permitted pixel-based analysis of thresholds defining infarction, using receiver operating characteristic curves. Results: Relative cerebral blood flow was the perfusion computed tomography parameter that most accurately predicted penumbra (area under the curve=0·698) and also infarct core (area under the curve=0·750). A relative cerebral blood flow threshold of <75% of mean contralateral cerebral blood flow most accurately predicted penumbral tissue at 0·5h (area under the curve=0·660), 1h (area under the curve=0·659), 1·5h (area under the curve=0·636), and 2h (area under the curve=0·664) after stroke onset. A relative cerebral blood flow threshold of <55% of mean contralateral most accurately predicted infarct core at 1h (area under the curve=0·765) and at 2h (area under the curve=0·689) after middle cerebral artery occlusion. Conclusions: The data provide perfusion computed tomography defined relative cerebral blood flow thresholds for infarct core and ischemic penumbra within the first two hours after experimental stroke in rats. These thresholds were shown to be stable to define the volume of infarct core and penumbra within this time window.

DOI 10.1111/ijs.12147
Citations Scopus - 10Web of Science - 11
Co-authors Mark Parsons, Lucy Murtha, Neil Spratt, Christopher Levi, Damian Mcleod
2015 Tomkins AJ, Hood RJ, Levi CR, Spratt NJ, 'Tissue Plasminogen Activator for preclinical stroke research: Neither "rat" nor "human" dose mimics clinical recanalization in a carotid occlusion model', SCIENTIFIC REPORTS, 5 (2015) [C1]
DOI 10.1038/srep16026
Citations Scopus - 5Web of Science - 5
Co-authors Christopher Levi, Neil Spratt
Show 2 more journal articles

Conference (7 outputs)

Year Citation Altmetrics Link
2017 Warren KE, Beard DJ, Hood RJ, Spratt NJ, 'Intracranial pressure elevation is delayed following intracerebral hemorrhage in rats', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY (2017)
Co-authors Neil Spratt
2017 Kovacs T, Murtha L, Beard D, McLeod D, Hood R, Garcia-Esperon C, et al., 'A potential cause of early neurological deterioration after mild-moderate ischaemic stroke - raised intracranial pressure at 24 hours', INTERNATIONAL JOURNAL OF STROKE (2017)
Co-authors Neil Spratt, Lucy Murtha, Damian Mcleod, Christopher Levi
2017 Hood RJ, McLeod DD, Warren KE, Pepperall D, Spratt NJ, 'Are there factors within cerebrospinal fluid that cause intracranial pressure to rise after subarachnoid hemorrhage?', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY (2017)
Co-authors Damian Mcleod, Neil Spratt
2016 McLeod DD, Murtha LA, Beard DJ, Hood RJ, Logan CL, Pepperall D, Spratt NJ, 'Elevated intracranial pressure following stroke: there's more to the story than cerebral oedema.', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vancouver, CANADA (2016)
Co-authors Lucy Murtha, Damian Mcleod, Neil Spratt
2016 Murtha L, Hood R, Beard D, Pepperall D, McLeod D, Spratt N, 'DELAYED INTRACRANIAL PRESSURE ELEVATION FOLLOWING ISCHEMIC STROKE IS PREVENTED BY EARLY AND SHORT HYPOTHERMIA TREATMENT IN AGED RATS', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vancouver, CANADA (2016)
Co-authors Neil Spratt
2016 Beard DJ, Logan CL, McLeod DD, Hood RJ, Pepperall D, Murtha LA, Spratt NJ, 'MIDDLE CEREBRAL ARTERY OCCLUSION WITH GOOD COLLATERALS CAUSES EARLY INTRACRANIAL PRESSURE ELEVATION POST STROKE', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vancouver, CANADA (2016)
Co-authors Damian Mcleod, Lucy Murtha, Neil Spratt
2016 Hood RJ, McLeod DD, Logan CL, Beard DJ, Li R, Spratt NJ, 'FACTOR(S) WITHIN CEREBROSPINAL FLUID POST-STROKE CAUSE INTRACRANIAL PRESSURE TO RISE IN HUMANS AND ANIMALS', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vancouver, CANADA (2016)
Co-authors Neil Spratt, Damian Mcleod
Show 4 more conferences
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Miss Rebecca Hood

Positions

Postdoctoral Researcher
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Casual Lecturer
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email rebecca.hood@newcastle.edu.au
Phone (02) 40420223

Office

Room Level 3 East
Building HMRI
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