Dr Daniel Beard

Dr Daniel Beard

Conjoint Lecturer

School of Biomedical Sciences and Pharmacy (Human Physiology)

Career Summary

Biography

Dr Daniel Beard completed his PhD (Human Physiology) in 2015 in the Translational Stroke Laboratory of Professor Neil Spratt at the University of Newcastle, Australia. His PhD thesis investigated the mechanisms regulating collateral blood flow after stroke. He found that changes in intracranial pressure (ICP) profoundly reduced collateral blood flow to the ischaemic brain during stroke. This work generated the novel hypothesis, that changes in ICP in human stroke may be the cause of the previously identified, but poorly understood phenomenon of collateral vessel failure and neurological deterioration in a subset of stroke patients. This work provided the stimulus for clinical investigations to the test this novel hypothesis.

In September 2016, Daniel was awarded a highly competitive postdoctoral fellowship in the laboratory of Professor Alastair Buchan, the Professor of Stroke Medicine and Pro-Vice Chancellor at the University of Oxford to work on a MRC UK funded project investigating the role of mammalian target of rapamycin mTOR in neurovascular dysfunction after stroke. In this role he continued to research the important role of the cerebral vasculature in determining stroke outcome. Specifically, he focused on targeting the  mTOR pathway to protect the cells that make up the capillaries of the brain as a means of improving microvascular perfusion, reducing blood brain barrier disruption and ultimately improving neurological outcome after stroke. Adjacent to this work he received a prestigious EMBO short-term fellowship and grant funding from the Berlin Institute of Health to visit the Charité  Universitätsmedizin in Berlin to establish a UK-European collaboration to investigate the role of the mTOR pathway in hypothermic neuroprotection in stroke. This project also served as a foundation to create a joint programme on neurovascular protection in stroke, as well as further foster the collaboration of the Charité with Oxford University. Daniel is continuing to collaborate with the scientists at Charite’ to continue this work. 

As well as his research pursuits, Daniel continued to develop his expertise as a university educator. While at Oxford he was appointed as a Lecturer in Medicine at Corpus Christi College and a Tutor in Physiology at Harris Manchester College. He also completed the Enhancing Teaching Programme in Sciences, a programme designed to support academic and research staff across the Medical Science Division who teach at Oxford to help improve their teaching and thus enhance their students’ learning experiences.  

Daniel was recently awarded an NHMRC Ideas Grant and has returned to the University of Newcastle as a lecturer to investigate novel therapies to enhance collateral blood flow after 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
  • Brain Cytoprotection
  • Cardiovascular Physiology
  • Cell Culture
  • Cerebrospinal Fluid
  • Collaterals
  • Computed Tomography Perfusion Imaging
  • Flow Cytometry
  • Higher Education Teaching
  • Hypothermia
  • Immunohistochemistry
  • Intracerebral Haemorrhage
  • Intracranial Pressure
  • Stress
  • Stroke
  • Systematic Review and Meta-analysis

Fields of Research

Code Description Percentage
060603 Animal Physiology - Systems 50
060805 Animal Neurobiology 25
060802 Animal Cell and Molecular Biology 25

Professional Experience

UON Appointment

Title Organisation / Department
Research Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
7/12/2009 - 25/6/2010 Research Assistant- Centre for Information Based Medicine Laboratory School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Australia
5/7/2010 - 28/1/2011 Research Assistant- Translational Stroke Laboratory School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Australia
27/8/2015 - 26/8/2016 Postdoctoral Researcher - Translational Stroke Laboratory Discipline of Human Physiology, School of Biomedical Sciences and Pharmacy, Faculty of health and Medicine, University of Newcastle
Australia
26/9/2016 - 31/10/2019 Postdoctoral Scientist in Acute Stroke - Laboratory of Cerebral Ischaemia University of Oxford
Radcliffe Department of Medicine
United Kingdom

Teaching appointment

Dates Title Organisation / Department
5/2/2007 - 26/6/2015 Casual Academic School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Australia
4/9/2017 - 8/3/2019 Lecturer in Medicine Corpus Christi College, University of Oxford
United Kingdom
4/9/2017 - 8/3/2019 Tutor in Physiology Harris Manchester College, University of Oxford
United Kingdom

Awards

Award

Year Award
2018 Guarantors of Brain Sponsorship Award for Short Meeting and Conferences: 8th Annual UK & Ireland Early Career Blood Brain Barrier Symposium, 30th of November 2018, Oxford.
University of Oxford

Distinction

Year Award
2009 University Medal
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

Prize

Year Award
2019 ISCBFM Early Career Investigator Travel Grant to attend the 29th International Symposium on Cerebral Blood Flow Metabolism and Function, Yokohama, Japan, 4-7th of July, 2019.
University of Oxford
2018 Oxford Berlin Summer School Travel Grant
University of Oxford
2018 Guarantors of Brain Travel Grant to attend the 11th World Stroke Congress in Montreal, Canada. October 17-20, 2018
University of Oxford
2015 ISCBFM Young Investigator Travel Grant to attend the 27th International Symposium on Cerebral Blood Flow, Metabolism and Function, Vancouver, Canada, 27 to 30th June, 2015.
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2012 3rd place in the University of Newcastle Three Minute Thesis Final
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2009 Biosystems Prize for Cellular and Molecular Science
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2009 ADInstruments Prize for Human Structure and Function
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2009 Biorad Prize for Biomedical Science
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

Research Award

Year Award
2015 School of Biomedical Sciences and Pharmacy Early Career Researcher Paper of the Month
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2013 Best student presentation, Kioloa Neuroscience Colloquium 2013
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

Scholarship

Year Award
2011 Australian Postgraduate Award, University of Newcastle
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2008 Biomedical Science Summer Vacation Scholarship
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
2007 University of Newcastle Summer Vacation Scholarship
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

Invitations

Committee Member

Year Title / Rationale
2019 Chair of the International Society of Cerebral Blood Flow and Metabolism Early Career Investigator Committee - Brain 2021
2018 International Society of Cerebral Blood Flow and Metabolism Early Career Investigator Committee - Brain 2019
2018 Founder and Chair of the Radcliffe Department of Medicine Researcher Association Committee
2017 Postdoctoral Representative on the Radcliffe Department of Medicine Career Development Committee
2017 Organizing committee for the 8th Annual UK & Ireland Early Career Blood Brain Barrier Symposium

Panel Participant

Year Title / Rationale
2018 Radcliffe Department of Medicine Award for Excellent Supervision Selection Panel
2017 Accelerated Medical Course interview panel, Harris Manchester College, University of Oxford

Peer Reviewer

Year Title / Rationale
2015 Hunter Medical Research Institute and Hunter Children’s Research Foundation Project Grant Review Panel.

Teaching

Code Course Role Duration
HUBS 1107 Neuroscience and Head and Neck Anatomy
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/7/2014 - 1/11/2014
MEDI 1015 Medical Science 1
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/3/2009 - 31/5/2015
HUBS 3403 Neuroscience
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/3/2015 - 31/5/2015
MEDI 3018 General Practice and Subspecialties 2
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/3/2009 - 31/5/2015
HUBS 1403 Biomedical Science Part 1
Faculty of Health, University of Newcastle
PASS Leader 
PASS Leader 1/3/2007 - 1/11/2008
MEDI 2014 Medical Science 3
Faculty of Health, University of Newcastle
Lab demonstrator
Casual Academic 1/3/2009 - 31/5/2015
HUBS 2105 Sports Science 2
Faculty of Health, University of Newcastle
Lab Demonstrator 
Casual Academic 1/3/2009 - 31/5/2012
HUBS1401 Human Biosciences
Faculty of Health, University of Newcastle
Casual tutor and lecturer. 
Casual Academic 1/3/2009 - 31/5/2015
BC98 Integrative Systems Physiology for Biomedical Science
Corpus Christi College, University of Oxford
Tutor 4/9/2017 - 8/3/2019
HUBS 1404 Biomedical Science Part 2
Faculty of Health, University of Newcastle
PASS Leader
PASS Leader 1/3/2007 - 1/11/2008
HUBS 1105 Musculoskeletal Anatomy
Faculty of Health, University of Newcastle
Lab Demonstrator
Casual Academic 1/3/2014 - 31/5/2015
A101 Physiology for Graduate Entry Medicine
Harris Manchester College, University of Oxford
Tutor 4/9/2017 - 8/3/2019
HUBS 2103 Neural and Visceral Anatomy
Faculty of Health, University of Newcastle
Lab demonstrator 
Casual Academic 1/3/2015 - 31/5/2015
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Publications

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


Journal article (12 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
Citations Scopus - 2Web of Science - 2
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
Citations Scopus - 1
2019 Hadley G, Beard DJ, Alexopoulou Z, Sutherland BA, Buchan AM, 'Investigation of the novel mTOR inhibitor AZD2014 in neuronal ischemia', Neuroscience Letters, 706 223-230 (2019)

© 2019 Elsevier B.V. Introduction: Hamartin, a component of the tuberous sclerosis complex (TSC) that actively inhibits the mammalian target of rapamycin (mTOR), may mediate the e... [more]

© 2019 Elsevier B.V. Introduction: Hamartin, a component of the tuberous sclerosis complex (TSC) that actively inhibits the mammalian target of rapamycin (mTOR), may mediate the endogenous resistance of Cornu Ammonis 3 (CA3) hippocampal neurons following global cerebral ischemia. Pharmacological compounds that selectively inhibit mTOR may afford neuroprotection following ischemic stroke. We hypothesize that AZD2014, a novel mTORC1/2 inhibitor, may protect neurons following oxygen and glucose deprivation (OGD). Methods: Primary neuronal cultures from E18 Wistar rat embryos were exposed to 2 h OGD or normoxia. AZD2014 was administered either during OGD, 24 h prior to OGD or for 24 h following OGD. Cell death was quantified by lactate dehydrogenase assay. We characterized the expression of mTOR pathway proteins following exposure to AZD2014 using western blotting. Results: Following 2 h OGD +24 h recovery, AZD2014 increased neuronal death when present during OGD. Rapamycin, the archetypal mTOR inhibitor, had no effect on cell death. Treatment with AZD2014 24 h prior to OGD and 24 h after OGD also enhanced cell death. While Western blotting showed a trend towards decreased expression levels of phospho-Akt relative to total Akt with increasing AZD2014 concentration, hamartin expression was also significantly decreased leading to activation of mTOR. Conclusion: AZD2014 was detrimental to neurons that underwent ischemia. AZD2014 appeared to reduce hamartin, a known neuroprotective mediator, thereby preventing any beneficial effects of mTOR inhibition. Further characterization of the role of individual mTOR complexes (mTORC1 and mTORC2) and their upstream and downstream regulators are necessary to reveal whether these pathways are neuroprotective targets for stroke.

DOI 10.1016/j.neulet.2019.05.023
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 - 6
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 - 7Web of Science - 5
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 - 7Web of Science - 5
Co-authors Neil Spratt, Rebecca Hood, Damian Mcleod, Lucy Murtha
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 - 5Web of Science - 5
Co-authors Lucy Murtha, 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 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 - 22Web of Science - 19
Co-authors Damian Mcleod, Lucy Murtha, 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 (&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 - 24Web of Science - 21
Co-authors Damian Mcleod, Lucy Murtha, Neil Spratt, Dirk Vanhelden
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 - 41Web 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 - 15Web of Science - 12
Co-authors Rohan Walker, Eugene Nalivaiko, Phillip Jobling
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 Neil Spratt, Christopher Levi, Damian Mcleod, Mark Parsons
Show 9 more journal articles

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, Rebecca Hood
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, Damian Mcleod, Christopher Levi, Lucy Murtha, Rebecca Hood
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, Rebecca Hood
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, Rebecca Hood, 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 Damian Mcleod, Rebecca Hood, Neil Spratt
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 Damian Mcleod, Neil Spratt
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 - 4Web of Science - 5
Co-authors Lucy Murtha, Neil Spratt, Damian Mcleod
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Grants and Funding

Summary

Number of grants 7
Total funding $493,064

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


20194 grants / $152,842

Neuroprotection: Is the mechanism of hypothermic neuroprotection explained by hamartin's effects on mTOR? $113,500

Funding body: Berlin Institute of Health

Funding body Berlin Institute of Health
Project Team

Alastair Buchan, Daniel Beard, Philipp Mergenthaler, Ulrich Dirnagl, Matthias Endres, Gabriele De Luca and Bryan Adriaanse.

Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo
Type Of Funding C3232 - International Govt - Other
Category 3232
UON N

Utilising shear-activated nanotherapeutics to selectively enhance collateral cerebral blood flow during stroke$18,842

Funding body: Medical Sciences Internal Fund - University of Oxford

Funding body Medical Sciences Internal Fund - University of Oxford
Project Team

Dr Daniel Beard, Professor Alastair Buchan, Dr Yvonne Couch, Dr Frank Bobe and Professor Donald Ingber

Scheme Pump Priming Award
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N

Investigating the role of hamartin in hypothermic neuroprotection in ischaemic stroke$10,500

Funding body: John Fell Fund - University of Oxford

Funding body John Fell Fund - University of Oxford
Project Team

Alastair Buchan, Daniel Beard, Gabriele De Luca, Bryan Adriaanse, Yvonne Couch

Scheme Small Grant Funding Scheme
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

EMBO Short-term Fellowship $10,000

Funding body: European Molecular Biology Organization

Funding body European Molecular Biology Organization
Project Team

Daniel Beard, Philipp Mergenthaler and Alastair Buchan

Scheme Short-term Fellowship Scheme
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

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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Research Supervision

Number of supervisions

Completed3
Current2

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2019 PhD Elucidating the Mechanisms Involved in Intracranial Pressure Elevation and Hypothermia Treatment for Ischaemic Stroke PhD (Human Physiology), Faculty of Health and Medicine, The University of Newcastle Consultant Supervisor
2019 PhD The metabolic effects of mTOR inhibition in stroke Biol Sc Not Elsewhere Classifd, University of Oxford Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2019 Honours Immunohistochemical Analysis of the Mammalian Target of Rapamycin Pathway in Human Hippocampi from Patients with Drug-Resistant Epilepsy Biol Sc Not Elsewhere Classifd, Oxford University, UK Principal Supervisor
2019 Honours Analysis of the Mechanistic Target of Rapamycin (mTOR) Pathway in the Human Cerebral Cortex after Ischaemic Stroke Biol Sc Not Elsewhere Classifd, University of Oxford Principal Supervisor
2018 Honours Investigating the Endogenous Neuroprotective Properties of Hamartin in Experimental Stroke Biol Sc Not Elsewhere Classifd, Oxford University, UK Principal Supervisor
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News

NHMRC awards $9.3 million to 13 University of Newcastle projects

December 18, 2019

The University of Newcastle has received more than $9.3 million in funding to support projects aiming to solve some of the world’s most critical health problems and improve the lives of millions of Australians.

Dr Daniel Beard

Positions

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

Research Fellow
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 7402
Fax (02) 4921 7903
Link Twitter

Office

Room MS508
Building Medical Sciences
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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