Dr Gabrielle Briggs

Dr Gabrielle Briggs

Postdoctoral Researcher and Lab Manager

School of Medicine and Public Health

Career Summary

Biography

Dr Briggs is the lead scientist working with the Trauma Service at the John Hunter Hospital and manages the Surgical Sciences Laboratory. Her research revolves around the complications and pathophysiology of severely injured patients, including coagulopathy, traumatic brain injury, sepsis, bone and joint infections, blood transfusions and tissue regeneration.

A theme to Dr Briggs’ research is working with clinicians to understand the problems they face, and applying her laboratory skills and biomedical knowledge to create novel, innovative solutions that can be translated to a real-world impact.

Some examples of her research projects include:

  • Development of a novel diagnostic test for rapid bacterial detection in sepsis and joint infection
  • Biomarker discovery for predicting outcome in traumatic brain injury
  • Novel biologicals for tissue regeneration
  • Novel approaches in transfusion medicine

Dr Briggs supervises/co-supervises a number of PhD students and Joint Medical Program Research Students working on the above projects.


Qualifications

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

Keywords

  • blood transfusion
  • flow cytometry
  • joint infection
  • mitochondria
  • molecular biology
  • orthopaedic surgery
  • post-injury inflammation
  • sepsis
  • traumatic injury

Fields of Research

Code Description Percentage
100404 Regenerative Medicine (incl. Stem Cells and Tissue Engineering) 30
110899 Medical Microbiology not elsewhere classified 30
110314 Orthopaedics 40

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Researcher and Lab Manager University of Newcastle
School of Medicine and Public Health
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (1 outputs)

Year Citation Altmetrics Link
2013 Dickson PW, Briggs GD, 'Tyrosine hydroxylase. Regulation by feedback inhibition and phosphorylation.', Advances in Pharmacology: A New Era of Catecholamines in the Laboratory and Clinic, Academic Press, San Diego 13-21 (2013) [B1]
DOI 10.1016/B978-0-12-411512-5.00002-6
Citations Scopus - 24
Co-authors Phil Dickson

Journal article (9 outputs)

Year Citation Altmetrics Link
2020 Briggs GD, Balogh ZJ, 'Tranexamic acid and inflammation in trauma', ANZ JOURNAL OF SURGERY, 90 426-428 (2020)
DOI 10.1111/ans.15755
Citations Scopus - 1
Co-authors Zsolt Balogh
2019 Amico F, Briggs G, Balogh ZJ, 'Transfused trauma patients have better outcomes when transfused with blood components from young donors', Medical Hypotheses, 122 141-146 (2019) [C1]

© 2018 The physiology of tissue healing and aging share common pathways. Both patient age and tissue healing are crucial factors predicting outcomes in trauma patients. The presen... [more]

© 2018 The physiology of tissue healing and aging share common pathways. Both patient age and tissue healing are crucial factors predicting outcomes in trauma patients. The presented hypothesis focuses on the concept that transfused trauma patients have better outcomes when transfused with blood components from young donors. The age of the donor of a blood transfusion could affect recovery following a major traumatic insult and help avoid postinjury immune paralysis and its associated complications. The frequent transfusion of blood components to the severely injured trauma patient provides an opportunity for the recipient to benefit from the potentially favourable effect of blood originating from young donors. Different types of evidence support the presented hypothesis including work on soluble circulating factors, research on animal parabiontic models and epidemiological studies. Theories on the role of transfusion of cells, on bone marrow and on senolytics also represent grounds to elaborate pathways to test this hypothesis. The precise molecular mechanism underlying this hypothesis is uncertain. A beneficial effect on trauma patients following transfusion of blood could be due to a positive effect of blood donated from younger donors or instead to the lack of a negative effect possibly occurring when transfusing blood from older donors. Either way, identifying this mechanism would provide a powerful tool enhance long and short term recovery after trauma.

DOI 10.1016/j.mehy.2018.11.016
Co-authors Zsolt Balogh
2018 Thurairajah K, Briggs GD, Balogh ZJ, 'The source of cell-free mitochondrial DNA in trauma and potential therapeutic strategies', European Journal of Trauma and Emergency Surgery, 44 325-334 (2018) [C1]

© 2018, The Author(s). Mitochondria play a key role in the pathophysiology of post-injury inflammation. Cell-free mitochondrial DNA (cf-mtDNA) is now understood to catalyse steril... [more]

© 2018, The Author(s). Mitochondria play a key role in the pathophysiology of post-injury inflammation. Cell-free mitochondrial DNA (cf-mtDNA) is now understood to catalyse sterile inflammation after trauma. Observations in trauma cohorts have identified high cf-mtDNA in patients with systemic inflammatory response syndrome and multiple organ failure as well as following major surgery. The source of cf-mtDNA can be various cells affected by mechanical and hypoxic injury (passive mechanism) or induced by inflammatory mechanisms (active mechanism). Multiple forms of cf-mtDNA exist; mtDNA fragments, mtDNA in microparticles/vesicles and cell-free mitochondria. Trauma to cells that are rich in mitochondria are believed to release more cf-mtDNA. This review describes the current understanding of the mechanisms of cf-mtDNA release, its systemic effects and the potential therapeutic implications related to its modification. Although current understanding is insufficient to change trauma management, focussed research goals have been identified to pave the way for monitoring and manipulation of cf-mtDNA release and effects in trauma.

DOI 10.1007/s00068-018-0954-3
Citations Scopus - 23Web of Science - 20
Co-authors Zsolt Balogh
2017 Ong LK, Page S, Briggs GD, Guan L, Dun MD, Verrills NM, et al., 'Peripheral Lipopolysaccharide Challenge Induces Long-Term Changes in Tyrosine Hydroxylase Regulation in the Adrenal Medulla', Journal of Cellular Biochemistry, 118 2096-2107 (2017) [C1]

© 2016 Wiley Periodicals, Inc. Immune activation can alter the activity of adrenal chromaffin cells. The effect of immune activation by lipopolysaccharide (LPS) on the regulation ... [more]

© 2016 Wiley Periodicals, Inc. Immune activation can alter the activity of adrenal chromaffin cells. The effect of immune activation by lipopolysaccharide (LPS) on the regulation of tyrosine hydroxylase (TH) in the adrenal medulla in vivo was determined between 1 day and 6 months after LPS injection. The plasma levels of eleven cytokines were reduced 1 day after LPS injection, whereas the level for interleukin-10 was increased. The levels of all cytokines remained at control levels until 6 months when the levels of interleukin-6 and -4 were increased. One day after LPS injection, there was a decrease in TH-specific activity that may be due to decreased phosphorylation of serine 31 and 40. This decreased phosphorylation of serine 31 and 40 may be due to an increased activation of the protein phosphatase PP2A. One week after LPS injection, there was increased TH protein and increased phosphorylation of serine 40 that this was not accompanied by an increase in TH-specific activity. All TH parameters measured returned to basal levels between 1 month and 3 months. Six months after injection there was an increase in TH protein. This was associated with increased levels of the extracellular regulated kinase isoforms 1 and 2. This work shows that a single inflammatory event has the capacity to generate both short-term and long-term changes in TH regulation in the adrenal medulla of the adult animal. J. Cell. Biochem. 118: 2096¿2107, 2017. © 2016 Wiley Periodicals, Inc.

DOI 10.1002/jcb.25839
Citations Scopus - 1Web of Science - 1
Co-authors Phil Dickson, Matt Dun, Peter Dunkley, Nikki Verrills, Linkooi Ong
2017 Tuboly E, McIlroy D, Briggs G, Lott N, Balogh ZJ, 'Clinical implications and pathological associations of circulating mitochondrial DNA', Frontiers in Bioscience - Landmark, 22 1011-1022 (2017) [C1]

Mitochondria are membrane-enclosed organelles, the energy-producing centers in almost all eukaryotic cells. The evolutionary emergence of mitochondria is a result of the endocytos... [more]

Mitochondria are membrane-enclosed organelles, the energy-producing centers in almost all eukaryotic cells. The evolutionary emergence of mitochondria is a result of the endocytosis of a-proteobacteria. There are several characteristic features which refer to its prokaryotic ancestors including its independent sets of double-stranded mitochondrial DNA, which is uniquely circular in form and contains a significant amount of unmethylated DNA as CpG islands. Resent research has proven that free mitochondrial DNA found in blood was associated with innate immunomodulation in a broad-range of clinical conditions. Upon release, mitochondrial DNA acts as a danger-associated molecular pattern in the circulation, it is recognized by pattern recognition receptors and it facilitates inflammatory responses. Besides its high receptor activation potential, mitochondrial DNA is likely to perform direct crosstalk with activated leukocytes and to be contributed to other anti-microbial activities. Here we highlight the pathological conditions where cell free mtDNA is involved, describe the potential sources and mechanisms of extracellular mtDNA release and explore evidence for its mechanism of action after being excreted and potential therapeutic strategies.

DOI 10.2741/4530
Citations Scopus - 7Web of Science - 6
Co-authors Zsolt Balogh
2014 Briggs GD, Bulley J, Dickson PW, 'Catalytic domain surface residues mediating catecholamine inhibition in tyrosine hydroxylase', Journal of Biochemistry, 155 183-193 (2014) [C1]
DOI 10.1093/jb/mvt110
Citations Scopus - 7Web of Science - 7
Co-authors Phil Dickson
2013 Briggs G, Bulley J, Dunkley PR, Dickson PW, 'Structural Basis for Regulation of Tyrosine Hydroxlyase by the Catecholamines 8-9 (2013) [E3]
DOI 10.1016/B978-0-12-800044-1.00006-4
Co-authors Phil Dickson, Peter Dunkley
2013 Briggs GD, Nagy GM, Dickson PW, 'Mechanism of action of salsolinol on tyrosine hydroxylase', Neurochemistry International, 63 726-731 (2013) [C1]

Tyrosine hydroxylase (TH) is the first and rate-limiting enzyme in dopamine synthesis. Dopamine regulates TH as an end-product inhibitor through its binding to a high and low affi... [more]

Tyrosine hydroxylase (TH) is the first and rate-limiting enzyme in dopamine synthesis. Dopamine regulates TH as an end-product inhibitor through its binding to a high and low affinity site, the former being abolished by Ser40 phosphorylation only, and the latter able to bind and dissociate according to intracellular dopamine levels. Here, we have investigated TH inhibition by a dopamine metabolite found in dopaminergic brain regions, salsolinol (SAL). SAL is known to decrease dopamine in the nigrostriatal pathway and mediobasal hypothalamus, and to also decrease plasma catecholamines in rat stress models, however a target and mechanism for the effects of SAL have not been found. We found that SAL inhibits TH activity in the nanomolar range in vitro, by binding to both the high and low affinity dopamine binding sites. SAL produces the same level of inhibition as dopamine when TH is non-phosphorylated. However, it produces 3.7-fold greater inhibition of Ser40-phosphorylated TH compared to dopamine by competing more strongly with tetrahydrobiopterin, the cofactor of this enzymatic reaction. SAL's potent inhibition of phosphorylated TH would prevent TH from being fully activated to synthesise dopamine. Crown Copyright © 2013 Published by Elsevier Ltd. All rights reserved.

DOI 10.1016/j.neuint.2013.09.016
Citations Scopus - 13Web of Science - 10
Co-authors Phil Dickson
2011 Briggs GD, Gordon SL, Dickson PW, 'Mutational analysis of catecholamine binding in tyrosine hydroxylase', Biochemistry, 50 1545-1555 (2011) [C1]
DOI 10.1021/bi101455b
Citations Scopus - 10Web of Science - 10
Co-authors Phil Dickson
Show 6 more journal articles

Conference (4 outputs)

Year Citation Altmetrics Link
2015 Ong LK, Briggs G, Guan L, Dunkley P, Dickson P, 'Inflammation and dopamine synthesis in neurodegeneration', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Co-authors Peter Dunkley, Linkooi Ong, Phil Dickson
2014 Ong LK, Briggs GD, Dunkley PR, Dickson PW, 'The role of inflammation and dopamine synthesis in Parkinson's disease', JOURNAL OF NEUROCHEMISTRY, Kaohsiung, TAIWAN (2014) [E3]
Co-authors Peter Dunkley, Phil Dickson, Linkooi Ong
2012 Briggs GD, Smith T, Hickey S, Dickson PW, 'A channel extending from the catalytic cleft of tyrosine hydroxylase is involved in high affinity catecholamine inhibition', Abstracts. Australian Neuroscience Society 32nd Annual Meeting, Gold Coast, Queensland (2012) [E3]
Co-authors Phil Dickson
2009 Briggs GD, Gordon SL, Dunkley PR, Dickson PW, 'Localisation of the low affinity catecholamine binding site in tyrosine hydroxylase', ANS 2009 Abstracts: Posters, Canberra, ACT (2009) [E3]
Co-authors Peter Dunkley, Phil Dickson
Show 1 more conference
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Grants and Funding

Summary

Number of grants 15
Total funding $224,659

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


20201 grants / $12,000

Development of a rapid diagnostic test to screen for septic patients in the emergency department$12,000

Funding body: John Hunter Charitable Trust Grant

Funding body John Hunter Charitable Trust Grant
Scheme John Hunter Charitable Trust Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

20194 grants / $80,008

Research into Advancing Traumatic Brain Injury Treatment$47,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Zsolt Balogh, Doctor Gabrielle Briggs
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900951
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Validation of a Novel Rapid Infection Diagnostic Test for Sepsis$17,307

Funding body: John Hunter Charitable Trust Grant

Funding body John Hunter Charitable Trust Grant
Scheme John Hunter Charitable Trust Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

Mitochondrial transfusion: a new biological therapy for non-union fracture healing$12,126

Funding body: AOTrauma Asia Pacific

Funding body AOTrauma Asia Pacific
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Development of an Early Sepsis Diagnostic Test$3,075

Funding body: School of Medicine and Public Health, The University of Newcastle

Funding body School of Medicine and Public Health, The University of Newcastle
Scheme SMPH Small Grant Round
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N

20181 grants / $2,391

Rapid Bacteria Detection in water sample$2,391

Funding body: Hunter Water Corporation

Funding body Hunter Water Corporation
Project Team Doctor Gabrielle Briggs, Professor Zsolt Balogh
Scheme Research Consultancy
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1801055
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

20174 grants / $39,683

To test the clinical applicability of a novel rapid and sensitive method for the diagnosis of septic arthritis$30,000

Funding body: AOA Australian Orthopaedic Association

Funding body AOA Australian Orthopaedic Association
Scheme Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding C1700 - Aust Competitive - Other
Category 1700
UON N

HMRI MRSP Secial Infrastructure Scheme - Early and Mid-Career Equipment Grant$4,183

Funding body: NSW Ministry of Health

Funding body NSW Ministry of Health
Project Team Professor Zsolt Balogh, Doctor Gabrielle Briggs, Doctor Steve Smith
Scheme Medical Research Support Program (MRSP)
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701285
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

Rapid Bacterial Detection - ON Prime3 Performance Grant$3,000

Funding body: CSIRO

Funding body CSIRO
Scheme ON Prime
Role Lead
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding C2120 - Aust Commonwealth - Other
Category 2120
UON N

Gordon Kerridge Memorial Scholarship$2,500

Funding body: John Hunter Hospital

Funding body John Hunter Hospital
Scheme Gordon Kerridge Memorial Scholarship
Role Lead
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Internal
Category INTE
UON N

20131 grants / $24,596

20121 grants / $1,500

Catecholamine Society Travel Fellowship$1,500

Funding body: Catecholamine Society

Funding body Catecholamine Society
Scheme Travel Fellowship
Role Lead
Funding Start 2012
Funding Finish 2012
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

20111 grants / $1,200

Travel Award: International Society for Neurochemistry Annual Scientific Meeting, Athens$1,200

Funding body: International Society for Neurochemistry

Funding body International Society for Neurochemistry
Scheme Travel Award Scheme
Role Lead
Funding Start 2011
Funding Finish 2011
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

20101 grants / $2,000

Research and Travel Grant: Runner Up, Inaugural Australia and New Zealand 3 Minute Thesis$2,000

Funding body: The University of Queensland

Funding body The University of Queensland
Scheme Inaugural Australia and New Zealand 3MT competition
Role Lead
Funding Start 2010
Funding Finish 2011
GNo
Type Of Funding C1700 - Aust Competitive - Other
Category 1700
UON N

20091 grants / $61,281

Australian Postgraduate Award$61,281

Funding body: Australian Federal Government

Funding body Australian Federal Government
Scheme Australian Postgraduate Award
Role Lead
Funding Start 2009
Funding Finish 2011
GNo
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON N
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Research Supervision

Number of supervisions

Completed0
Current4

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2020 PhD Massive Transfusion Protocol, Post Trauma Multiple Organ Failure and Inflammatory Responses PhD (Trauma Sciences), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2019 PhD Influence of Shock and Systemic Inflammation on Fracture Union PhD (Trauma Sciences), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2018 PhD Molecular Response to Trauma PhD (Surgical Science), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2018 PhD Effect of Blood Products Donor Demographics on Transfused Trauma Patients' Outcome PhD (Trauma Sciences), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Dr Gabrielle Briggs

Position

Postdoctoral Researcher and Lab Manager
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email gabrielle.briggs@newcastle.edu.au
Phone (02) 49 214495

Office

Room RM 3203, Department of Surgery, John Hunter Hospital
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