Dr Daniel Beard
Senior Lecturer
School of Biomedical Sciences and Pharmacy (Human Physiology)
- Email:daniel.j.beard@newcastle.edu.au
- Phone:(02) 4055 0790
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 |
---|---|---|
310906 | Animal neurobiology | 25 |
310910 | Animal physiology - systems | 50 |
310902 | Animal cell and molecular biology | 25 |
Professional Experience
UON Appointment
Title | Organisation / Department |
---|---|
Senior Lecturer | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Academic appointment
Dates | Title | Organisation / Department |
---|---|---|
26/9/2016 - 31/10/2019 | Postdoctoral Scientist in Acute Stroke - Laboratory of Cerebral Ischaemia | University of Oxford Radcliffe Department of Medicine United Kingdom |
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 |
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 |
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 |
Teaching appointment
Dates | Title | Organisation / Department |
---|---|---|
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 |
5/2/2007 - 26/6/2015 | Casual Academic | School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle Australia |
Awards
Award
Year | Award |
---|---|
2022 |
Paul Dudley White International Scholar Award University of Newcastle |
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 |
Guarantors of Brain Travel Grant to attend the 11th World Stroke Congress in Montreal, Canada. October 17-20, 2018 University of Oxford |
2018 |
Oxford Berlin Summer School Travel Grant 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 |
Biorad Prize for Biomedical 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 |
Biosystems Prize for Cellular and Molecular 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 | Organizing committee for the 8th Annual UK & Ireland Early Career Blood Brain Barrier Symposium |
2017 | Postdoctoral Representative on the Radcliffe Department of Medicine Career Development Committee |
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 |
---|---|
2020 | NHMRC Ideas Grants 2020 |
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 |
HUBS3204 |
Biomedical Research Integrated Learning School of Biomedical Sciences and Pharmacy |
Lecturer | 1/2/2021 - 30/6/2021 |
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 |
PHAR2102 |
Cardiovascular and Renal Health School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle |
Course Coordinator | 18/7/2022 - 16/12/2022 |
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 |
HUBS3414 |
Anatomical Pathology School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle |
Lecturer | 1/7/2021 - 1/12/2021 |
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 |
HUBS2507 |
Integrative Physiology for Biomedical Science The University of Newcastle |
Lecturer | 27/7/2020 - 30/11/2020 |
HUBS2505 |
Human Pathophysiology Universtiy of Newcastle |
Lecturer | 2/3/2020 - 30/6/2020 |
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 |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (27 outputs)
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2023 |
Hood RJ, Beard DJ, McLeod DD, Murtha LA, Spratt NJ, 'Intracranial pressure elevation post-stroke: Mechanisms and consequences', Frontiers in Stroke, 2 [C1]
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2023 |
Hood RJ, Sanchez-Bezanilla S, Beard DJ, Rust R, Turner RJ, Stuckey SM, et al., 'Leakage beyond the primary lesion: A temporal analysis of cerebrovascular dysregulation at sites of hippocampal secondary neurodegeneration following cortical photothrombotic stroke', Journal of Neurochemistry, 167 733-752 (2023) [C1] We have previously demonstrated that a cortical stroke causes persistent impairment of hippocampal-dependent cognitive tasks concomitant with secondary neurodegenerative processes... [more] We have previously demonstrated that a cortical stroke causes persistent impairment of hippocampal-dependent cognitive tasks concomitant with secondary neurodegenerative processes such as amyloid-ß accumulation in the hippocampus, a region remote from the primary infarct. Interestingly, there is emerging evidence suggesting that deposition of amyloid-ß around cerebral vessels may lead to cerebrovascular structural changes, neurovascular dysfunction, and disruption of blood¿brain barrier integrity. However, there is limited knowledge about the temporal changes of hippocampal cerebrovasculature after cortical stroke. In the current study, we aimed to characterise the spatiotemporal cerebrovascular changes after cortical stroke. This was done using the photothrombotic stroke model targeting the motor and somatosensory cortices of mice. Cerebrovascular morphology as well as the co-localisation of amyloid-ß with vasculature and blood¿brain barrier integrity were assessed in the cortex and hippocampal regions at 7, 28 and 84 days post-stroke. Our findings showed transient cerebrovascular remodelling in the peri-infarct area up to 28 days post-stroke. Importantly, the cerebrovascular changes were extended beyond the peri-infarct region to the ipsilateral hippocampus and were sustained out to 84 days post-stroke. When investigating vessel diameter, we showed a decrease at 84 days in the peri-infarct and CA1 regions that were exacerbated in vessels with amyloid-ß deposition. Lastly, we showed sustained vascular leakage in the peri-infarct and ipsilateral hippocampus, indicative of a compromised blood¿brain-barrier. Our findings indicate that hippocampal vasculature may represent an important therapeutic target to mitigate the progression of post-stroke cognitive impairment.
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2023 |
Adriaanse BA, Brady S, Wang M, Beard DJ, Spencer JI, Pansieri J, et al., 'Tuberous sclerosis complex-1 (TSC1) contributes to selective neuronal vulnerability in Alzheimer's disease', Neuropathology and Applied Neurobiology, 49 (2023) [C1]
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2022 |
Zhu WM, Neuhaus A, Beard DJ, Sutherland BA, DeLuca GC, 'Neurovascular coupling mechanisms in health and neurovascular uncoupling in Alzheimer s disease', Brain, 145 2276-2292 (2022) [C1]
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2022 |
Sanchez-Bezanilla S, Beard DJ, Hood RJ, Åberg ND, Crock P, Walker FR, et al., 'Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice.', Neural plasticity, 2022 9983042 (2022) [C1]
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2021 |
Omileke D, Pepperall D, Bothwell SW, Mackovski N, Azarpeykan S, Beard DJ, et al., 'Ultra-Short Duration Hypothermia Prevents Intracranial Pressure Elevation Following Ischaemic Stroke in Rats', FRONTIERS IN NEUROLOGY, 12 (2021) [C1]
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2021 |
Omileke D, Azarpeykan S, Bothwell SW, Pepperall D, Beard DJ, Coupland K, et al., 'Short-duration hypothermia completed prior to reperfusion prevents intracranial pressure elevation following ischaemic stroke in rats', SCIENTIFIC REPORTS, 11 (2021) [C1]
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2021 |
Omileke D, Bothwell SW, Pepperall D, Beard DJ, Coupland K, Patabendige A, Spratt NJ, 'Decreased Intracranial Pressure Elevation and Cerebrospinal Fluid Outflow Resistance: A Potential Mechanism of Hypothermia Cerebroprotection Following Experimental Stroke', Brain Sciences, 11 (2021) [C1]
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2021 |
Omileke D, Bothwell S, Beard D, MacKovski N, Azarpeykan S, Coupland K, et al., 'Short-duration hypothermia induction in rats using
models for studies examining clinical relevance and
mechanisms', Journal of Visualized Experiments, 169 (2021) [C1]
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2020 |
Beard DJ, Brown LS, Sutherland BA, 'The rise of pericytes in neurovascular research', Journal of Cerebral Blood Flow and Metabolism, 40 2366-2373 (2020) [C1] The popularity of pericyte research is increasing, and this was not more evident than at the recent 2019 Brain meeting in Yokohama which featured a large number of presentations f... [more] The popularity of pericyte research is increasing, and this was not more evident than at the recent 2019 Brain meeting in Yokohama which featured a large number of presentations focused on brain pericyte research, including the Presidential Symposium. In this article, we will provide a history of brain pericyte research, present the results of our analysis showing a substantial increase in brain pericyte research presented at Brain meetings since 2005, suggest reasons for their increased popularity, and comment on what the future holds for brain pericyte research.
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2020 |
Beard DJ, Li Z, Schneider AM, Couch Y, Cipolla MJ, Buchan AM, 'Rapamycin Induces an eNOS (Endothelial Nitric Oxide Synthase) Dependent Increase in Brain Collateral Perfusion in Wistar and Spontaneously Hypertensive Rats', Stroke, 51 2834-2843 (2020) [C1] Background and Purpose: Rapamycin is a clinically approved mammalian target of rapamycin inhibitor that has been shown to be neuroprotective in animal models of stroke. However, t... [more] Background and Purpose: Rapamycin is a clinically approved mammalian target of rapamycin inhibitor that has been shown to be neuroprotective in animal models of stroke. However, the mechanism of rapamycin-induced neuroprotection is still being explored. Our aims were to determine if rapamycin improved leptomeningeal collateral perfusion, to determine if this is through eNOS (endothelial nitric oxide synthase)-mediated vessel dilation and to determine if rapamycin increases immediate postreperfusion blood flow. Methods: Wistar and spontaneously hypertensive rats (¿14 weeks old, n=22 and n=15, respectively) were subjected to ischemia by middle cerebral artery occlusion (90 and 120 minutes, respectively) with or without treatment with rapamycin at 30-minute poststroke. Changes in middle cerebral artery and collateral perfusion territories were measured by dual-site laser Doppler. Reactivity to rapamycin was studied using isolated and pressurized leptomeningeal anastomoses. Brain injury was measured histologically or with triphenyltetrazolium chloride staining. Results: In Wistar rats, rapamycin increased collateral perfusion (43±17%), increased reperfusion cerebral blood flow (16±8%) and significantly reduced infarct volume (35±6 versus 63±8 mm3, P<0.05). Rapamycin dilated leptomeningeal anastomoses by 80±9%, which was abolished by nitric oxide synthase inhibition. In spontaneously hypertensive rats, rapamycin increased collateral perfusion by 32±25%, reperfusion cerebral blood flow by 44±16%, without reducing acute infarct volume 2 hours postreperfusion. Reperfusion cerebral blood flow was a stronger predictor of brain damage than collateral perfusion in both Wistar and spontaneously hypertensive rats. Conclusions: Rapamycin increased collateral perfusion and reperfusion cerebral blood flow in both Wistar and comorbid spontaneously hypertensive rats that appeared to be mediated by enhancing eNOS activation. These findings suggest that rapamycin may be an effective acute therapy for increasing collateral flow and as an adjunct therapy to thrombolysis or thrombectomy to improve reperfusion blood flow.
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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) [C1] Introduction: Hamartin, a component of the tuberous sclerosis complex (TSC) that actively inhibits the mammalian target of rapamycin (mTOR), may mediate the endogenous resistance ... [more] 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.
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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) [C1] Background: Amplifying endogenous neuroprotective mechanisms is a promising avenue for stroke therapy. One target is mammalian target of rapamycin (mTOR), a serine/threonine kinas... [more] 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.
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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) [C1]
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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) [C1] 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 me... [more] 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.
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2016 |
Beard DJ, Murtha LA, McLeod DD, Spratt NJ, 'Intracranial Pressure and Collateral Blood Flow', Stroke, 47 1695-1700 (2016) [C1]
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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]
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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]
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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] 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 equa... [more] 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.
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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] Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite st... [more] 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.
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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)
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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)
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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.
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Nova | |||||||||
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]
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Nova | |||||||||
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]
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Nova | |||||||||
Show 24 more journal articles |
Conference (16 outputs)
Year | Citation | Altmetrics | Link | ||
---|---|---|---|---|---|
2022 | Beard D, El Amki M, Prado AV, Glueck C, Nelson MT, Coelho-Santos V, Liebeskind D, 'Brain vasculature: Architecture, collaterals and capillaries', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Glasgow, SCOTLAND (2022) | ||||
2022 |
Litman M, Azarpeykan S, Uzun O, Bhatta D, Buchan A, Spratt N, et al., 'Shear-activated nanotherapeutics to selectively increase leptomeningeal collateral blood flow during ischemic stroke', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Glasgow, SCOTLAND (2022)
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2022 |
Beard D, Hough N, Esperon CG, Lillicrap T, Djenidi L, Spratt N, 'Computational fluid dynamic analysis of leptomeningeal collateral blood flow shear stress in ischaemic stroke patients', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Glasgow, SCOTLAND (2022)
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2013 |
Beard D, McLeod D, Spratt N, 'The collateral circulation: key to outcome in mice and men', INTERNATIONAL JOURNAL OF STROKE (2013) [E3]
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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]
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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]
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Show 13 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]
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Preprint (3 outputs)
Year | Citation | Altmetrics | Link | |||||
---|---|---|---|---|---|---|---|---|
2024 |
Beard DJ, Brown LS, Morris GP, Couch Y, Adriaanse BA, Karali CS, et al., 'Rapamycin Treatment Reduces Brain Pericyte Constriction in Ischemic Stroke (2024)
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2023 |
Hood RJ, Sanchez-Bezanilla S, Beard DJ, Rust R, Turner RJ, Stuckey SM, et al., 'Leakage beyond the primary infarction: A temporal analysis of cerebrovascular dysregulation at sites of hippocampal secondary neurodegeneration following cortical photothrombotic stroke (2023)
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2023 |
Schneider AM, Couch Y, Larkin J, Buchan AM, Beard DJ, 'Post-stroke rapamycin treatment improves post-recanalization cerebral blood flow and outcome in rats (2023)
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Grants and Funding
Summary
Number of grants | 16 |
---|---|
Total funding | $1,101,916 |
Click on a grant title below to expand the full details for that specific grant.
20235 grants / $113,467
Investigating the ‘no reflow’ phenomenon in a clinically relevant model of stroke$48,327
Funding body: Neurosurgical Research Foundation
Funding body | Neurosurgical Research Foundation |
---|---|
Project Team | Rebecca Hood, Garry Morris, Daniel Beard, Brad Sutherland, Tracy Farr |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2024 |
GNo | |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | N |
Assessment of the safety and efficacy of shear-activated nanotherapeutics to selectively enhance leptomeningeal collateral blood flow in stroke$36,000
Funding body: Brain Foundation (NSW Branch)
Funding body | Brain Foundation (NSW Branch) |
---|---|
Project Team | Doctor Daniel Beard, Prof Donald Ingber, Professor Donald Ingber, Dr Neal Muni, Dr Neal Muni, Professor Neil Spratt |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2200727 |
Type Of Funding | C1700 - Aust Competitive - Other |
Category | 1700 |
UON | Y |
Investigation of cerebral blood flow changes in regions of secondary neurodegeneration following ischaemic stroke$19,716
Funding body: HMRi Heart and Stroke Research Program
Funding body | HMRi Heart and Stroke Research Program |
---|---|
Project Team | Daniel Beard, Marina Paul, Rohan Walker, Lizzie Manning, Lin Ong, Rebecca Hood |
Scheme | 2023 EMCR Pilot Study Funding Round |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
External collaboration_International_Beard$5,802
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Daniel Beard |
Scheme | External Collaboration Grant Scheme - International |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2300436 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Do statins increase cerebral collateral angiogenesis?$3,622
Funding body: College of Health Medicine and Wellbeing
Funding body | College of Health Medicine and Wellbeing |
---|---|
Project Team | Kirsten Coupland, Daniel Beard, Neil Spratt |
Scheme | Strategic Pilot Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20221 grants / $5,000
Investigating the role of pericytes in leptomeningeal collateral vessel function$5,000
Funding body: NSW Cardiovascular Research Network
Funding body | NSW Cardiovascular Research Network |
---|---|
Project Team | Neil Spratt, Brad Sutherland |
Scheme | VCCRI Research Innovation Grant |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2023 |
GNo | |
Type Of Funding | C1600 - Aust Competitive - StateTerritory Govt |
Category | 1600 |
UON | N |
20211 grants / $10,217
Investigating the role of pericytes in leptomeningeal collateral vessel function$10,217
Funding body: College of Health, Medicine and Wellbeing
Funding body | College of Health, Medicine and Wellbeing |
---|---|
Project Team | Dr Daniel Beard, Professor Neil Spratt, Associate Professor Brad Sutherland |
Scheme | Strategic Research Pilot Grant |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20202 grants / $480,168
Shear-activated nanotherapeutics to selectively enhance collateral cerebral blood flow during ischaemic stroke$475,168
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Daniel Beard, Professor Neil Spratt, Professor Donald Ingber |
Scheme | Ideas Grants |
Role | Lead |
Funding Start | 2020 |
Funding Finish | 2022 |
GNo | G1900437 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Laser Speckle Contrast Imager (LSCI) for imaging of perfusion in cerebral and peripheral vasculature in experimental models of Stroke and Peripheral Vascular Disease (PVD)$5,000
Funding body: School of Biomedical Sciences and Pharmacy
Funding body | School of Biomedical Sciences and Pharmacy |
---|---|
Project Team | Daniel Beard, Neil Spratt, Michael Bourke |
Scheme | SBSP Equipment Grant |
Role | Lead |
Funding Start | 2020 |
Funding Finish | 2020 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
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 | C3200 – Aust Not-for Profit |
Category | 3200 |
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 |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2020 | PhD | Shear-activated Nanotherapeutics to Selectively Enhance Collateral Cerebral Blood Flow during Ischaemic Stroke | PhD (Human Physiology), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2022 | PhD | Elucidating the Mechanisms Involved in Intracranial Pressure Elevation and Hypothermia Treatment for Ischaemic Stroke | PhD (Human Physiology), College of Health, Medicine and Wellbeing, The University of Newcastle | Consultant Supervisor |
2022 | PhD | The metabolic effects of mTOR inhibition in stroke | Biol Sc Not Elsewhere Classifd, University of Oxford | Co-Supervisor |
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 |
Research Collaborations
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
Country | Count of Publications | |
---|---|---|
Australia | 37 | |
United Kingdom | 20 | |
United States | 6 | |
Switzerland | 2 | |
Malaysia | 2 | |
More... |
News
News • 18 Dec 2019
NHMRC awards $9.3 million to 13 University of Newcastle projects
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
Position
Senior Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Focus area
Human Physiology
Contact Details
daniel.j.beard@newcastle.edu.au | |
Phone | (02) 4055 0790 |
Mobile | 0491650516 |
Fax | (02) 4921 7903 |
Link |
Office
Room | MS507 |
---|---|
Building | Medical Sciences |
Location | Callaghan University Drive Callaghan, NSW 2308 Australia |