Dr Daniel Beard

Dr Daniel Beard

Conjoint Lecturer

School of Biomedical Sciences and Pharmacy (Human Physiology)

Career Summary

Biography

I have recently completed my PhD in human physiology in the Translational Stroke Lab of Neil Spratt at the University of Newcastle, the same lab in which I am currently employed as a postdoctoral researcher. My main interests are both cardiovascular physiology and neuroscience, in particular how the cardiovascular system affects the functioning of the nervous system. This ultimately lead to me to my current research area of stroke, a disease in which disruption of blood supply to the brain has a profound and often devastating effect on brain function leading death and disability. 

My current research interests/expertise include: Cerebral ischaemia/Stroke; The influence of the leptomeningeal collateral circulation on the ischaemic penumbra and stroke outcome; Measuring brain perfusion (ischaemic penumbra) using Perfusion Computed Tomography (CTP) after stroke; Effects of intracranial pressure (ICP) elevation on leptomeningeal collateral blood flow and brain perfusion during experimental stroke; Mechanisms of hypothermic neuroprotection following ischaemic stroke; investigating changes in cerebrospinal fluid dynamics after ischaemic stroke. 


Qualifications

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

Keywords

  • Autonomic Nervous System
  • Cardiovascular Physiology
  • Cerebrospinal Fluid
  • Collaterals
  • Computed Tomography Perfusion Imaging
  • Hypothermia
  • Intracerebral Haemorrhage
  • Intracranial Pressure
  • Stress
  • Stroke

Fields of Research

Code Description Percentage
060603 Animal Physiology - Systems 25
060805 Animal Neurobiology 35
110399 Clinical Sciences not elsewhere classified 40

Teaching

Code Course Role Duration
MEDI 2014 Medical Science 3
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/03/2009 - 31/05/2015
MEDI 3018 General Practice and Subspecialties 2
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/03/2009 - 31/05/2015
HUBS 1403 Biomedical Science Part 1
Faculty of Health, University of Newcastle
PASS Leader 
PASS Leader 1/03/2007 - 1/11/2008
HUBS 1404 Biomedical Science Part 2
Faculty of Health, University of Newcastle
PASS Leader
PASS Leader 1/03/2007 - 1/11/2008
HUBS1401 Human Biosciences
Faculty of Health, University of Newcastle
Casual tutor and lecturer. 
Casual Academic 1/03/2009 - 31/05/2015
HUBS 1107 Neuroscience and Head and Neck Anatomy
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/07/2014 - 1/11/2014
HUBS 1105 Musculoskeletal Anatomy
Faculty of Health, University of Newcastle
Lab Demonstrator
Casual Academic 1/03/2014 - 31/05/2015
HUBS 2105 Sports Science 2
Faculty of Health, University of Newcastle
Lab Demonstrator 
Casual Academic 1/03/2009 - 31/05/2012
HUBS 2103 Neural and Visceral Anatomy
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/03/2015 - 31/05/2015
HUBS 3403 Neuroscience
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/03/2015 - 31/05/2015
MEDI 1015 Medical Science 1
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/03/2009 - 31/05/2015
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Publications

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


Journal article (11 outputs)

Year Citation Altmetrics Link
2019 Hadley G, Beard DJ, Couch Y, Neuhaus AA, Adriaanse BA, DeLuca GC, et al., 'Rapamycin in ischemic stroke: Old drug, new tricks?', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 39 20-35 (2019)
DOI 10.1177/0271678X18807309
2019 Beard DJ, Hadley G, Thurley N, Howells DW, Sutherland BA, Buchan AM, 'The effect of rapamycin treatment on cerebral ischemia: A systematic review and meta-analysis of animal model studies', International Journal of Stroke, 14 137-145 (2019)

© 2018 World Stroke Organization. Background: Amplifying endogenous neuroprotective mechanisms is a promising avenue for stroke therapy. One target is mammalian target of rapamyci... [more]

© 2018 World Stroke Organization. Background: Amplifying endogenous neuroprotective mechanisms is a promising avenue for stroke therapy. One target is mammalian target of rapamycin (mTOR), a serine/threonine kinase regulating cell proliferation, cell survival, protein synthesis, and autophagy. Animal studies investigating the effect of rapamycin on mTOR inhibition following cerebral ischemia have shown conflicting results. Aim: To conduct a systematic review and meta-analysis evaluating the effectiveness of rapamycin in reducing infarct volume in animal models of ischemic stroke. Summary of review: Our search identified 328 publications. Seventeen publications met inclusion criteria (52 comparisons: 30 reported infarct size and 22 reported neurobehavioral score). Study quality was modest (median 4 of 9) with no evidence of publication bias. The point estimate for the effect of rapamycin was a 21.6% (95% CI, 7.6%¿35.7% p < 0.01) improvement in infarct volume and 30.5% (95% CI 17.2%¿43.8%, p < 0.0001) improvement in neuroscores. Effect sizes were greatest in studies using lower doses of rapamycin. Conclusion: Low-dose rapamycin treatment may be an effective therapeutic option for stroke. Modest study quality means there is a potential risk of bias. We recommend further high-quality preclinical studies on rapamycin in stroke before progressing to clinical trials.

DOI 10.1177/1747493018816503
2018 Hadley G, Neuhaus AA, Couch Y, Beard DJ, Adriaanse BA, Vekrellis K, et al., 'The role of the endoplasmic reticulum stress response following cerebral ischemia', International Journal of Stroke, 13 379-390 (2018)

© 2017, © 2017 World Stroke Organization. Background: Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnera... [more]

© 2017, © 2017 World Stroke Organization. Background: Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability. Methods: In¿vivo: male Wistar rats underwent sham or 10 min of transient global cerebral ischemia. CA1 and CA3 areas were microdissected and endoplasmic reticulum stress protein expression quantified at 3 h and 12 h of reperfusion. In¿vitro: primary neuronal cultures (E18 Wistar rat embryos) were exposed to 2 h of oxygen and glucose deprivation or normoxia in the presence of an endoplasmic reticulum stress inducer (thapsigargin or tunicamycin), an endoplasmic reticulum stress inhibitor (salubrinal or 4-phenylbutyric acid), an autophagy inducer ([4'-(N-diethylamino) butyl]-2-chlorophenoxazine (10-NCP)) or autophagy inhibitor (3-methyladenine). Results: In¿vivo, decreased endoplasmic reticulum stress protein expression (phospho-eIF2a and ATF4) was observed at 3 h of reperfusion in CA3 neurons following ischemia, and increased in CA1 neurons at 12 h of reperfusion. In¿vitro, endoplasmic reticulum stress inducers and high doses of the endoplasmic reticulum stress inhibitors also increased cell death. Both induction and inhibition of autophagy also increased cell death. Conclusion: Endoplasmic reticulum stress is associated with neuronal cell death following ischemia. Neither reduction of endoplasmic reticulum stress nor induction of autophagy demonstrated neuroprotection in¿vitro, highlighting their complex role in neuronal biology following ischemia.

DOI 10.1177/1747493017724584
Citations Scopus - 2
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 - 4Web of Science - 4
Co-authors Damian Mcleod, Neil Spratt, Lucy Murtha
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 - 5Web of Science - 3
Co-authors Damian Mcleod, Lucy Murtha, Neil Spratt
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 - 3Web of Science - 3
Co-authors Damian Mcleod, Lucy Murtha, 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 af... [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 measured 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 - 19Web of Science - 14
Co-authors Neil Spratt, Lucy Murtha, Damian Mcleod
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 (&apos;collateral failure&apos;) is associated with late infarct expan... [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 driven 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 - 20Web of Science - 17
Co-authors Neil Spratt, Dirk Vanhelden, Lucy Murtha, Damian Mcleod
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 - 31Web of Science - 16
Co-authors Christopher Levi, Neil Spratt, Lucy Murtha, Damian Mcleod, Mark Parsons
2013 Bobrovskaya L, Beard D, Bondarenko E, Beig MI, Jobling P, Walker FR, et al., 'Does exposure to chronic stress influence blood pressure in rats?', AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL, 177 217-223 (2013) [C1]
DOI 10.1016/j.autneu.2013.05.001
Citations Scopus - 13Web of Science - 11
Co-authors Rohan Walker, Phillip Jobling, Eugene Nalivaiko
2013 McLeod DD, Beard DJ, Parsons MW, Levi CR, Calford MB, Spratt NJ, 'Inadvertent Occlusion of the Anterior Choroidal Artery Explains Infarct Variability in the Middle Cerebral Artery Thread Occlusion Stroke Model', PLOS ONE, 8 (2013) [C1]
DOI 10.1371/journal.pone.0075779
Citations Scopus - 8Web of Science - 9
Co-authors Mark Parsons, Damian Mcleod, Neil Spratt, Christopher Levi
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Conference (8 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 Christopher Levi, Lucy Murtha, 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 Damian Mcleod, Lucy Murtha, 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
2013 Beard D, McLeod D, Spratt N, 'The collateral circulation: key to outcome in mice and men', INTERNATIONAL JOURNAL OF STROKE (2013) [E3]
Co-authors Neil Spratt, Damian Mcleod
2012 Beard DJ, McLeod DD, Imtiaz MS, Spratt NJ, 'Quantitative assessment of leptomeningeal collateral flow in experimental stroke', The Stroke Interventionalist, Los Angeles, CA (2012) [E3]
Co-authors Damian Mcleod, Neil Spratt
2012 McLeod DD, Beard DJ, Imtiaz MS, Spratt NJ, 'Validating a novel method for measuring leptomeningeal collateral flow in experimental stroke', The Stroke Interventionalist, Los Angeles, CA (2012) [E3]
Co-authors Neil Spratt, Damian Mcleod
Show 5 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 - 3Web of Science - 3
Co-authors Neil Spratt, Lucy Murtha, Damian Mcleod
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Grants and Funding

Summary

Number of grants 3
Total funding $340,222

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


20153 grants / $340,222

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 C3112 - Aust Not for profit
Category 3112
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

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
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Dr Daniel Beard

Position

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

Focus area

Human Physiology

Contact Details

Email daniel.j.beard@newcastle.edu.au
Phone (02) 4921 7303
Fax (02) 4921 7903

Office

Room MS504
Building Medical Sciences
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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