Dr Lucy Murtha

Dr Lucy Murtha

Post-doctoral Scholar

School of Medicine and Public Health

Career Summary

Biography

Dr Murtha is a Postdoctoral Research Scholar in the School of Medicine and Public Health at the University of Newcastle. Dr Murtha’s current research interests involve understanding the molecular mechanisms of cardiac fibrosis, a devastating consequence of almost every cardiac disease, of which treatment options are inadequate. She is interested in using pre-clinical models of cardiovascular disease to find effective ways of reversing the devastating effects heart scarring.

Dr Murtha completed a Bachelor of Biomedical Science (Honours) and a Doctor of Philosophy (PhD) at the University of Newcastle, Australia. Her PhD thesis investigated the mechanisms causing pressure to rise in the skull (intracranial pressure) following experimental stroke and the benefits of using therapeutic body cooling (hypothermia) to prevent this dangerous rise in pressure. The data collected throughout her PhD changed the current understanding of intracranial pressure regulation after stroke and the use of short-term hypothermia as a therapy. Dr Murtha is closely involved with further preclinical and clinical investigations which are currently underway.

Dr Murtha was recently awarded the Australian Government’s prestigious, competitive, merit-based Endeavour fellowship, which provided the opportunity to visit and collaborate with a world-leading laboratory at the University of Toronto, Canada. She was also awarded the Australian Society for Medical Research International award to collaborate with the world-leading cardiovascular institute, the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Spain.

Dr Murtha’s PhD was generously supported by an Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship. The provision of this scholarship allowed her to travel to the University of Glasgow, UK, to conduct an international collaborative project for 12 months. This project resulted in the fascinating discovery that the major cause of the elevated pressure after stroke was not due to brain swelling, as was previously assumed, and lead a high impact journal article which went on to win the Best Research Higher Degree Publication of the Month, and of the Year by the School of Biomedical Sciences and Pharmacy, and the Faculty of Health and Medicine, respectively at the RHD Excellence Awards, 2015. Dr Murtha’s PhD thesis abstract was nominated by the University of Newcastle to be published in the Journal and Proceedings of the Royal Society of New South Wales. 


Qualifications

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

Keywords

  • Biomedical Sciences - Cardiology
  • Biomedical Sciences - Neuroscience
  • Cardiac Fibrosis
  • Cardiovascular Disease
  • Extracellular Matrix
  • Heart Failure
  • Intracranial Pressure
  • Ischaemic Stroke
  • Left Ventricular Remodelling
  • Medical Physiology
  • Oedema (cerebral)
  • Pre-clinical Models of Cardiovascular Disease
  • Therapeutic Hypothermia

Fields of Research

Code Description Percentage
110201 Cardiology (incl. Cardiovascular Diseases) 75
060603 Animal Physiology - Systems 25

Professional Experience

UON Appointment

Title Organisation / Department
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Post-doctoral Scholar University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
20/04/2015 - 4/04/2016 Postdoctoral Researcher Discipline of Human Physiology, School of Biomedical Sciences and Pharmacy, Faculty of health and Medicine, 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 (14 outputs)

Year Citation Altmetrics Link
2017 Rostas JAP, Hoffman A, Murtha LA, Pepperall D, McLeod DD, Dickson PW, et al., 'Ischaemia- and excitotoxicity-induced CaMKII-Mediated neuronal cell death: The relative roles of CaMKII autophosphorylation at T286 and T253.', Neurochem Int, 104 6-10 (2017)
DOI 10.1016/j.neuint.2017.01.002
Citations Scopus - 1Web of Science - 2
Co-authors Kathryn Skelding, Damian Mcleod, Phil Dickson, Neil Spratt, John Rostas
2016 Murtha LA, 'The effects and mechanisms of the therapeutic hypothermia on intracranial pressure regulation following ischaemic stroke in rats', Journal and Proceedings of the Royal Society of New South Wales, 149 101-102 (2016)
2016 Beard DJ, Murtha LA, McLeod DD, Spratt NJ, 'Intracranial Pressure and Collateral Blood Flow', Stroke, 47 1695-1700 (2016) [C1]
DOI 10.1161/STROKEAHA.115.011147
Citations Scopus - 2Web of Science - 3
Co-authors Damian Mcleod, 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 - 1Web of Science - 3
Co-authors Neil Spratt, Damian Mcleod
2016 Murtha LA, Beard DJ, Bourke JT, Pepperall D, McLeod DD, Spratt NJ, 'Intracranial Pressure Elevation 24 h after Ischemic Stroke in Aged Rats Is Prevented by Early, Short Hypothermia Treatment.', Front Aging Neurosci, 8 124 (2016) [C1]
DOI 10.3389/fnagi.2016.00124
Citations Scopus - 1Web of Science - 1
Co-authors Damian Mcleod, Neil Spratt
2015 Murtha LA, McLeod DD, Pepperall D, McCann SK, Beard DJ, Tomkins AJ, et al., 'Intracranial pressure elevation after ischemic stroke in rats: Cerebral edema is not the only cause, and short-duration mild hypothermia is a highly effective preventive therapy', Journal of Cerebral Blood Flow and Metabolism, 35 592-600 (2015) [C1]

© 2015 ISCBFM All rights reserved. In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation a... [more]

© 2015 ISCBFM All rights reserved. In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35 °C) or moderate (32.5 °C) hypothermia, or normothermia (37 °C) was induced after stroke onset. Edema was me asured in three studies, using wet-dry weight calculations, T 2-weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ¿ICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset.

DOI 10.1038/jcbfm.2014.230
Citations Scopus - 11Web of Science - 11
Co-authors Damian Mcleod, Neil Spratt
2015 Beard DJ, Mcleod DD, Logan CL, Murtha LA, Imtiaz MS, Van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke', Journal of Cerebral Blood Flow and Metabolism, 35 861-872 (2015) [C1]

© 2015 ISCBFM. Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expa... [more]

© 2015 ISCBFM. Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by > 450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driv en by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.

DOI 10.1038/jcbfm.2015.2
Citations Scopus - 9Web of Science - 11
Co-authors Neil Spratt, Dirk Vanhelden, Damian Mcleod
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 (isc... [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 - 7Web of Science - 7
Co-authors Damian Mcleod, Christopher Levi, Neil Spratt, Mark Parsons
2015 Tomkins AJ, Schleicher N, Murtha L, Kaps M, Levi CR, Nedelmann M, Spratt NJ, 'Platelet rich clots are resistant to lysis by thrombolytic therapy in a rat model of embolic stroke', Experimental and Translational Stroke Medicine, 7 (2015) [C1]

© 2015 Tomkins et al. Background: Early recanalization of occluded vessels in stroke is closely associated with improved clinical outcome. Microbubble-enhanced sonothrombolysis i... [more]

© 2015 Tomkins et al. Background: Early recanalization of occluded vessels in stroke is closely associated with improved clinical outcome. Microbubble-enhanced sonothrombolysis is a promising therapy to improve recanalization rates and reduce the time to recanalization. Testing any thrombolytic therapy requires a model of thromboembolic stroke, but to date these models have been highly variable with regards to clot stability. Here, we developed a model of thromboembolic stroke in rats with site-specific delivery of platelet-rich clots (PRC) to the main stem of the middle cerebral artery (MCA). This model was used in a subsequent study to test microbubble-enhanced sonothrombolysis. Methods: In Study 1 we investigated spontaneous recanalization rates of PRC in vivo over 4 hours and measured infarct volumes at 24 hours. In Study 2 we investigated tPA-mediated thrombolysis and microbubble-enhanced sonothrombolysis in this model. Results: Study 1 demonstrated stable occlusion out to 4 hours in 5 of 7 rats. Two rats spontaneously recanalized at 40 and 70 minutes post-embolism. Infarct volumes were not significantly different in recanalized rats, 43.93 ± 15.44% of the ischemic hemisphere, compared to 48.93 ± 3.9% in non-recanalized animals (p = 0.7). In Study 2, recanalization was not observed in any of the groups post-treatment. Conclusions: Site specific delivery of platelet rich clots to the MCA origin resulted in high rates of MCA occlusion, low rates of spontaneous clot lysis and large infarction. These platelet rich clots were highly resistant to tPA with or without microbubble-enhanced sonothrombolysis. This resistance of platelet rich clots to enhanced thrombolysis may explain recanalization failures clinically and should be an impetus to better clot-type identification and alternative recanalization methods.

DOI 10.1186/s13231-014-0014-y
Citations Scopus - 7
Co-authors Neil Spratt, Christopher Levi
2014 Beard DJ, McLeod DD, Murtha LA, Spratt NJ, 'Elevation of intracranial pressure reduces leptomeningeal collateral and watershed blood flow during experimental stroke', CEREBROVASCULAR DISEASES, 37 65-65 (2014)
Co-authors Damian Mcleod, Neil Spratt
2014 Murtha LA, McLeod DD, Beard DJ, Pepperall DG, Spratt NJ, 'Short duration mild hypothermia prevents delayed intracranial pressure rise following experimental ischaemic stroke', CEREBROVASCULAR DISEASES, 37 340-340 (2014)
Co-authors Damian Mcleod, Neil Spratt
2014 Murtha LA, Mcleod DD, Mccann SK, Pepperall D, Chung S, Levi CR, et al., 'Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise', International Journal of Stroke, 9 553-559 (2014) [C1]

Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Thera... [more]

Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Therapeutic hypothermia improves outcome after cardiac arrest, is strongly neuroprotective in experimental stroke, and is under clinical trial in stroke. Hypothermia lowers elevated intracranial pressure; however, rebound intracranial pressure elevation and neurological deterioration may occur during rewarming. Hypotheses: (1) Intracranial pressure increases 24h after moderate and small strokes. (2) Short-duration hypothermia-rewarming, instituted before intracranial pressure elevation, prevents this 24h intracranial pressure elevation. Methods: Long-Evans rats with two hour middle cerebral artery occlusion or outbred Wistar rats with three hour middle cerebral artery occlusion had intracranial pressure measured at baseline and 24h. Wistars were randomized to 2·5h hypothermia (32·5°C) or normothermia, commencing 1h after stroke. Results: In Long-Evans rats (n=5), intracranial pressure increased from 10·9±4·6mmHg at baseline to 32·4±11·4mmHg at 24h, infarct volume was 84·3±15·9mm 3 . In normothermic Wistars (n=10), intracranial pressure increased from 6·7±2·3mmHg to 31·6±9·3mmHg, infarct volume was 31·3±18·4mm 3 . In hypothermia-treated Wistars (n=10), 24h intracranial pressure did not increase (7·0±2·8mmHg, P < 0·001 vs. normothermia), and infarct volume was smaller (15·4±11·8mm 3 , P < 0·05). Conclusions: We saw major intracranial pressure elevation 24h after stroke in two rat strains, even after small strokes. Short-duration hypothermia prevented the intracranial pressure rise, an effect sustained for at least 18h after rewarming. The findings have potentially important implications for design of future clinical trials. © 2013 The Authors. International Journal of Stroke © 2013 World Stroke Organization.

DOI 10.1111/ijs.12181
Citations Scopus - 14Web of Science - 13
Co-authors Damian Mcleod, Christopher Levi, Neil Spratt
2014 Murtha LA, Yang Q, Parsons MW, Levi CR, Beard DJ, Spratt NJ, McLeod DD, 'Cerebrospinal fluid is drained primarily via the spinal canal and olfactory route in young and aged spontaneously hypertensive rats', Fluids and Barriers of the CNS, 11 (2014) [C1]

Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the... [more]

Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the route of CSF drainage. Our aim was to quantify CSF flow, volume, and drainage route dynamics in vivo in young and aged spontaneously hypertensive rats (SHR) using a novel contrast-enhanced computed tomography (CT) method.Methods: ICP was recorded in young (2-5 months) and aged (16 months) SHR. Contrast was administered into the lateral ventricles bilaterally and sequential CT imaging was used to visualize the entire intracranial CSF system and CSF drainage routes. A customized contrast decay software module was used to quantify CSF flow at multiple locations.Results: ICP was significantly higher in aged rats than in young rats (11.52 ± 2.36 mmHg, versus 7.04 ± 2.89 mmHg, p = 0.03). Contrast was observed throughout the entire intracranial CSF system and was seen to enter the spinal canal and cross the cribriform plate into the olfactory mucosa within 9.1 ± 6.1 and 22.2 ± 7.1 minutes, respectively. No contrast was observed adjacent to the sagittal sinus. There were no significant differences between young and aged rats in either contrast distribution times or CSF flow rates. Mean flow rates (combined young and aged) were 3.0 ± 1.5 µL/min at the cerebral aqueduct; 3.5 ± 1.4 µL/min at the 3rd ventric= and 2.8 ± 0.9 µL/min at the 4th ventricle. Intracranial CSF volumes (and as percentage total brain volume) were 204 ± 97 µL (8.8 ± 4.3%) in the young and 275 ± 35 µL (10.8 ± 1.9%) in the aged animals (NS).Conclusions: We have demonstrated a contrast-enhanced CT technique for measuring and visualising CSF dynamics in vivo. These results indicate substantial drainage of CSF via spinal and olfactory routes, but there was little evidence of drainage via sagittal sinus arachnoid granulations in either young or aged animals. The data suggests that spinal and olfactory routes are the primary routes of CSF drainage and that sagittal sinus arachnoid granulations play a minor role, even in aged rats with higher ICP. © 2014 Murtha et al.; licensee BioMed Central Ltd.

DOI 10.1186/2045-8118-11-12
Citations Scopus - 15
Co-authors Damian Mcleod, Mark Parsons, Christopher Levi, Neil Spratt
2012 Murtha L, McLeod D, Spratt N, 'Epidural intracranial pressure measurement in rats using a fiber-optic pressure transducer.', Journal of visualized experiments : JoVE, (2012) [C1]
Citations Scopus - 12Web of Science - 1
Co-authors Damian Mcleod, Neil Spratt
Show 11 more journal articles

Conference (6 outputs)

Year Citation Altmetrics Link
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 (2016)
Co-authors Damian Mcleod, 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 (2016)
Co-authors Damian Mcleod, Neil Spratt
2015 Rostas J, Hoffman A, Murtha L, Pepperall D, McLeod D, Dickson P, et al., 'Ischaemia-induced neuronal cell death is mediated by molecular targeting of CaMKII phosphorylated at T253', JOURNAL OF NEUROCHEMISTRY (2015) [E3]
Co-authors Kathryn Skelding, Neil Spratt, Damian Mcleod, Phil Dickson, John Rostas
2012 Murtha LA, McLeod DD, Spratt NJ, 'The effects of therapeutic hypothermia on intracranial pressure after experimental ischemic stroke', Abstracts. Australian Neuroscience Society 32nd Annual Meeting (2012) [E3]
Co-authors Damian Mcleod, Neil Spratt
2012 McLeod DD, Murtha LA, Pitsillides K, 'A new method of attaching a solid-state pressure sensor for measurement of chronic intracranial pressure in freely moving rats using biotelemetry', FASEB Journal (2012) [E3]
Co-authors Damian Mcleod
2011 Murtha LA, McLeod DD, McCann S, Pepperall D-G, Spratt NJ, 'Short duration hypothermia results in sustained prevention of intracranial pressure elevation following experimental stroke', International Journal of Stroke (2011) [E3]
Co-authors Neil Spratt, Damian Mcleod
Show 3 more conferences

Other (1 outputs)

Year Citation Altmetrics Link
2015 Murtha LA, Mcleod DD, Pepperall D, Mccann SK, Beard DJ, Tomkins AJ, et al., 'Erratum: Intracranial pressure elevation after ischemic stroke in rats: Cerebral edema is not the only cause, and short-duration mild hypothermia is a highly effective preventive therapy (Journal of Cerebral Blood Flow & Metabolism (2015) 35 (592-600) DOI: 10.1038/jcbfm.2014.230)', ( issue.12 pp.2109) (2015) [O1]
DOI 10.1038/jcbfm.2015.209
Citations Scopus - 1Web of Science - 2
Co-authors Damian Mcleod, Neil Spratt
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Grants and Funding

Summary

Number of grants 11
Total funding $521,064

Click on a grant title below to expand the full details for that specific grant.


20175 grants / $142,000

Characterising the role of Fibulin-3 in health and disease$67,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lucy Murtha, Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2018
GNo G1700327
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Determining the mechanisms of cardiac fibrosis$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lucy Murtha
Scheme Greaves Family Early Career Support Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700352
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Endeavour Research Fellowship$24,500

Funding body: Department of Education and Training

Funding body Department of Education and Training
Scheme Endeavour Research Fellowship
Role Lead
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON N

Identifying the role of fibulin-3 in cardiac fibrosis$20,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Lucy Murtha, Dr Rohan Bhagwandeen, Dr Rachel Hatton
Scheme Research Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700475
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

ASMR Travel Grant$5,000

Funding body: Australian Society for Medical Research (ASMR)

Funding body Australian Society for Medical Research (ASMR)
Scheme International Travel Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON N

20161 grants / $4,000

Characterising the role of fibulin-3 in health and disease$4,000

Funding body: UON, Faculty Health and Medicine

Funding body UON, Faculty Health and Medicine
Scheme Faculty Health and Medicine
Role Lead
Funding Start 2016
Funding Finish 2016
GNo
Type Of Funding Internal
Category INTE
UON N

20155 grants / $375,064

A new understanding of increased pressure within the skull in brain diseases$300,000

Funding body: Brain Foundation (NSW Branch)

Funding body Brain Foundation (NSW Branch)
Project Team Professor Neil Spratt, Doctor Damian McLeod, Doctor Lucy Murtha, Doctor Daniel Beard
Scheme Major Research Gift Initiative
Role Investigator
Funding Start 2015
Funding Finish 2017
GNo G1501106
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Stroke In Progression: a new understanding of pathophysiology opening the door to effective therapy$25,222

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Ferdinand Miteff, Doctor Damian McLeod, Doctor Daniel Beard, Doctor Lucy Murtha, Professor Neil Spratt
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500830
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Cooling the blood to prevent raised intracranial pressure and improve outcome after stroke$19,842

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Lucy Murtha, Professor Neil Spratt
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500591
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

A better understanding of intracranial pressure changes after brain injury$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Neil Spratt, Doctor Damian McLeod, Doctor Lucy Murtha, Doctor Daniel Beard
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2017
GNo G1500709
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

A better understanding of intracranial pressure changes after brain injury$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team

Doctor Neil Spratt

Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON N
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Research Supervision

Number of supervisions

Completed0
Current1

Total current UON EFTSL

PhD0.2

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD The Identification of Novel Proteins Expressed by Human Cardiac Stem and Progenitor Cells to Develop Regenerative Non-Cellular Therapies for Heart Failure PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Opportunities

Investigating cardiac fibrosis in ageing and heart disease

Research Project Opportunities

Honours

School of Medicine and Public Health

1/01/2018 - 31/12/2018

Contact

Doctor Lucy Murtha
University of Newcastle
School of Medicine and Public Health
lucy.murtha@newcastle.edu.au

Investigating cardiac fibrosis in ageing and heart disease

Research Project Opportunities

Honours

School of Medicine and Public Health

1/01/2018 - 31/12/2018

Contact

Doctor Lucy Murtha
University of Newcastle
School of Medicine and Public Health
lucy.murtha@newcastle.edu.au

Investigating cardiac fibrosis in ageing and heart disease

Research Project Opportunities

PHD

School of Medicine and Public Health

1/01/2018 - 31/12/2020

Contact

Doctor Lucy Murtha
University of Newcastle
School of Medicine and Public Health
lucy.murtha@newcastle.edu.au

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News

PHD Scholarship: Cardiovascular research

September 25, 2017

The Priority Clinical Centre for Cardiovascular Health currently has an opportunity for a new PhD student to receive a fully funded scholarship to research cardiovascular health, under the supervision of Dr Lucy Murtha and Professor Andrew Boyle.

PhD Opportunity: Extracellular matrix protein in pressure overload-induced cardiac fibrosis

July 3, 2017

The Priority Clinical Centre for Cardiovascular Health is seeking expressions of interest for a motivated student to investigate the role of a novel extracellular matrix protein in pressure overload-induced cardiac fibrosis, under the supervision of Professor Andrew Boyle and Dr Lucy Murtha.

Masters Opportunity: Investigating a novel injectable polymer for cardiac regeneration

June 29, 2017

The Priority Clinical Centre for Cardiovascular Health is seeking expressions of interest for a highly motivated student to conduct a Research Masters project investigating novel injectable polymer for cardiac regeneration under the supervision of Professor Andrew Boyle and Dr Lucy Murtha.

Dr Lucy Murtha

Positions

Post-doctoral Scholar
School of Medicine and Public Health
Faculty of Health and Medicine

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

Contact Details

Email lucy.murtha@newcastle.edu.au
Link Research Networks

Office

Room HMRI Level 3 East
Building Hunter Medical Research Institute
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