Dr Jason Girkin

Dr Jason Girkin

Associate Lecturer

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Jason complete a first class research honours degree in 2011 in the Bachelor of Biomedical Sciences and Pharmacy, focusing on the role of early life rhinovirus infections and pattern recognition receptor signalling and the interface between maladaptive innate immunity in the development of asthma. After completing his honours degree, Jason went on to conduct PhD studies in Immunology and Microbiology. His thesis focused on the role of rhinovirus infection and novel molecular signalling pathways in asthma exacerbations and was the culmination of four original scientific journal article publications from throughout his PhD candidature, supported by the Australian Post Graduate Award scholarship and the Vice Chancellors Award top-up scholarship.
Jason's post-doctoral career has focused on innate immunity in the lung, antiviral responses and novel therapeutics for prophylactic treatment of viral-induced disease. 

Qualifications

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

Keywords

  • Asthma
  • Innate Immunity
  • Rhinovirus

Fields of Research

Code Description Percentage
320499 Immunology not elsewhere classified 100

Professional Experience

UON Appointment

Title Organisation / Department
Associate Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Associate Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Teaching

Code Course Role Duration
PHAR6704 Pharmacology of Chronic Conditions
The University of Newcastle - School of Biomedical Sciences and Pharmacy
This course provides students with knowledge of the pharmacological management of chronic conditions, and the effects of long term drug administration on an individual. The course will emphasise application of this knowledge to specific case examples relevant to students of allied health professions.
Lecturer 22/2/2021 - 4/6/2021
MEDI1101B Year 1 JMP MD PBL Tutorials
Faculty of Health and Medicine, University of Newcastle

Overview of the Immune System Functino

Introduction to microbes, microbiota and infections

Associate Lecturer 27/3/2019 - 28/3/2019
MEDI2101A Clinical Sciences, Scholarship and Practice 2 Part A
Faculty of Health and Medicine, University of Newcastle
Pathogenesis of autoimmune processes in the nervous system
Associate Lecturer - Biomedical Sciences Content 24/5/2019 - 25/5/2019
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Publications

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


Chapter (2 outputs)

Year Citation Altmetrics Link
2019 Girkin J, Maltby S, Singanayagam A, Bartlett N, Malia P, 'In vivo experimental models of infection and disease', Rhinovirus infections and disease: Rethinking impact on human health and disease, Elsevier, London 195-238 (2019) [B1]
DOI 10.1016/B978-0-12-816417-4.00008-1
Co-authors Nathan Bartlett, Steven Maltby
2019 McLean G, Girkin J, Solari R, 'Emerging therapeutic approaches', Rhinovirus Infections: Rethinking the Impact on Human Health and Disease, Elsevier, London 239-263 (2019) [B1]
DOI 10.1016/B978-0-12-816417-4.00009-3

Journal article (9 outputs)

Year Citation Altmetrics Link
2021 Deliyannis G, Wong CY, McQuilten HA, Bachem A, Clarke M, Jia X, et al., 'TLR2-mediated activation of innate responses in the upper airways confers antiviral protection of the lungs', JCI Insight, 6 (2021) [C1]

The impact of respiratory virus infections on global health is felt not just during a pandemic, but endemic seasonal infections pose an equal and ongoing risk of severe disease. M... [more]

The impact of respiratory virus infections on global health is felt not just during a pandemic, but endemic seasonal infections pose an equal and ongoing risk of severe disease. Moreover, vaccines and antiviral drugs are not always effective or available for many respiratory viruses. We investigated how induction of effective and appropriate antigen-independent innate immunity in the upper airways can prevent the spread of respiratory virus infection to the vulnerable lower airways. Activation of TLR2, when restricted to the nasal turbinates, resulted in prompt induction of innate immune¿driven antiviral responses through action of cytokines, chemokines, and cellular activity in the upper but not the lower airways. We have defined how nasal epithelial cells and recruitment of macrophages work in concert and play pivotal roles to limit progression of influenza virus to the lungs and sustain protection for up to 7 days. These results reveal underlying mechanisms of how control of viral infection in the upper airways can occur and support the implementation of strategies that can activate TLR2 in nasal passages to provide rapid protection, especially for at-risk populations, against severe respiratory infection when vaccines and antiviral drugs are not always effective or available.

DOI 10.1172/jci.insight.140267
Co-authors Nathan Bartlett
2021 Girkin J, Loo S-L, Esneau C, Maltby S, Mercuri F, Chua B, et al., 'TLR2-mediated innate immune priming boosts lung anti-viral immunity.', The European respiratory journal, 58 (2021)
DOI 10.1183/13993003.01584-2020
Citations Web of Science - 2
Co-authors Andrew Reid, Nathan Bartlett, Peter Wark, Christopher Grainge, Punnam Veerati, Darryl Knight, Steven Maltby
2020 Sokulsky LA, Garcia-Netto K, Nguyen TH, Girkin JLN, Collison A, Mattes J, et al., 'A critical role for the CXCL3/CXCL5/CXCR2 neutrophilic chemotactic axis in the regulation of type 2 responses in a model of rhinoviral-induced asthma exacerbation', Journal of Immunology, 205 2468-2478 (2020)
DOI 10.4049/jimmunol.1901350
Citations Scopus - 2Web of Science - 3
Co-authors Paul Foster, Nathan Bartlett, Ming Yang, Adam Collison, Gerard Kaiko, Joerg Mattes
2019 Singanayagam A, Loo SL, Calderazzo M, Finney LJ, Torralbo MBT, Bakhsoliani E, et al., 'Antiviral immunity is impaired in COPD patients with frequent exacerbations', American Journal of Physiology - Lung Cellular and Molecular Physiology, 317 L893-L903 (2019) [C1]

Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine t... [more]

Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine the innate immune mechanisms that underlie susceptibility to frequent exacerbations in COPD. We measured sputum expression of immune mediators and bacterial loads in samples from patients with COPD at stable state and during virusassociated exacerbations. In vitro immune responses to rhinovirus infection in differentiated primary bronchial epithelial cells (BECs) sampled from patients with COPD were additionally evaluated. Patients were stratified as frequent exacerbators (=2 exacerbations in the preceding year) or infrequent exacerbators (<2 exacerbations in the preceding year) with comparisons made between these groups. Frequent exacerbators had reduced sputum cell mRNA expression of the antiviral immune mediators type I and III interferons and reduced interferon-stimulated gene (ISG) expression when clinically stable and during virus-associated exacerbation. A role for epithelial cellintrinsic innate immune dysregulation was identified: induction of interferons and ISGs during in vitro rhinovirus (RV) infection was also impaired in differentiated BECs from frequent exacerbators. Frequent exacerbators additionally had increased sputum bacterial loads at 2 wk following virus-associated exacerbation onset. These data implicate deficient airway innate immunity involving epithelial cells in the increased propensity to exacerbations observed in some patients with COPD. Therapeutic approaches to boost innate antimicrobial immunity in the lung could be a viable strategy for prevention and treatment of frequent exacerbations.

DOI 10.1152/ajplung.00253.2019
Citations Scopus - 17Web of Science - 16
Co-authors Nathan Bartlett, Andrew Reid, Punnam Veerati, Prabuddha Pathinayake, Christopher Grainge, Peter Wark
2018 Singanayagam A, Glanville N, Girkin JL, Ching YM, Marcellini A, Porter JD, et al., 'Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations', NATURE COMMUNICATIONS, 9 (2018) [C1]
DOI 10.1038/s41467-018-04574-1
Citations Scopus - 62Web of Science - 62
Co-authors Peter Wark, Punnam Veerati, Andrew Reid, Nathan Bartlett, Christopher Grainge, Prabuddha Pathinayake, Darryl Knight
2017 Girkin JL, Hatchwell LM, Collison AM, Starkey MR, Hansbro PM, Yagita H, et al., 'TRAIL signaling is proinflammatory and proviral in a murine model of rhinovirus 1B infection', American Journal of Physiology - Lung Cellular and Molecular Physiology, 312 L89-L99 (2017) [C1]

The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAI... [more]

The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient (Tnfsf10-/-) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10-/-mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection. Chemokines were quantified by ELISA of whole lung lysates and viral load was determined by quantitative RT-PCR and tissue culture infective dose (TCID50). Human airway epithelial cells (BEAS2B) were infected with RV1B and stimulated with recombinant TRAIL or neutralizing anti-TRAIL antibodies and viral titer assessed by TCID50. HDM-challenged Tnfsf10-/-mice were protected against RV-induced AHR and had suppressed cellular infiltration in the airways upon RV infection. Chemokine C-X-C-motif ligand 2 (CXCL2) production was suppressed in naïve Tnfsf10-/-mice infected with RV1B, with less RV1B detected 24 h postinfection. This was associated with reduced apoptotic cell death and a reduction of interferon (IFN)-¿2/3 but not IFN-a or IFN-ß. TRAIL stimulation increased, whereas anti-TRAIL antibodies reduced viral replication in RV1B-infected BEAS2B cells in vitro. In conclusion, TRAIL promotes RV-induced AHR, inflammation and RV1B replication, implicating this molecule and its downstream signaling pathways as a possible target for the amelioration of RV1B-induced allergic and nonallergic lung inflammation and AHR.

DOI 10.1152/ajplung.00200.2016
Citations Scopus - 11Web of Science - 11
Co-authors Philip Hansbro, Malcolm Starkey, Adam Collison, Paul Foster, Joerg Mattes
2015 Hatchwell L, Collison A, Girkin J, Parsons K, Li J, Zhang J, et al., 'Toll-like receptor 7 governs interferon and inflammatory responses to rhinovirus and is suppressed by IL-5-induced lung eosinophilia', Thorax, (2015) [C1]

© 2015 BMJ Publishing Group Ltd &amp; British Thoracic Society.Background Asthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), w... [more]

© 2015 BMJ Publishing Group Ltd & British Thoracic Society.Background Asthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), which is sensed by Toll-like receptors (TLR) such as TLR7. Some asthmatics have impaired interferon (IFN) responses to RV, but the underlying mechanisms of this clinically relevant observation are poorly understood. Objectives To investigate the importance of intact TLR7 signalling in vivo during RV exacerbation using mouse models of house dust mite (HDM)-induced allergic airways disease exacerbated by a superimposed RV infection. Methods Wild-type and TLR7-deficient (Tlr7<sup>-/-</sup>) BALB/c mice were intranasally sensitised and challenged with HDM prior to infection with RV1B. In some experiments, mice were administered recombinant IFN or adoptively transferred with plasmacytoid dendritic cells (pDC). Results Allergic Tlr7<sup>-/-</sup> mice displayed impaired IFN release upon RV1B infection, increased virus replication and exaggerated eosinophilic inflammation and airways hyper reactivity. Treatment with exogenous IFN or adoptive transfer of TLR7-competent pDCs blocked these exaggerated inflammatory responses and boosted IFN? release in the absence of host TLR7 signalling. TLR7 expression in the lungs was suppressed by allergic inflammation and by interleukin (IL)-5-induced eosinophilia in the absence of allergy. Subjects with moderate-to-severe asthma and eosinophilic but not neutrophilic airways inflammation, despite inhaled steroids, showed reduced TLR7 and IFN?2/3 expression in endobronchial biopsies. Furthermore, TLR7 expression inversely correlated with percentage of sputum eosinophils. Conclusions This implicates IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression and antiviral responses, which provides a molecular mechanism underpinning the effect of eosinophil-targeting treatments for the prevention of asthma exacerbations.

DOI 10.1136/thoraxjnl-2014-205465
Citations Scopus - 61Web of Science - 58
Co-authors Joerg Mattes, Nathan Bartlett, Adam Collison, Darryl Knight, Peter Wark, Paul Foster
2015 Girkin J, Hatchwell L, Foster P, Johnston SL, Bartlett N, Collison A, Mattes J, 'CCL7 and IRF-7 mediate hallmark inflammatory and IFN responses following rhinovirus 1B infection', Journal of Immunology, 194 4924-4930 (2015) [C1]

Rhinovirus (RV) infections are common and have the potential to exacerbate asthma. We have determined the lung transcriptome in RV strain 1B-infected naive BALB/c mice (nonallergi... [more]

Rhinovirus (RV) infections are common and have the potential to exacerbate asthma. We have determined the lung transcriptome in RV strain 1B-infected naive BALB/c mice (nonallergic) and identified CCL7 and IFN regulatory factor (IRF)-7 among the most upregulated mRNA transcripts in the lung. To investigate their roles we employed anti-CCL7 Abs and an IRF-7-targeting small interfering RNA in vivo. Neutralizing CCL7 or inhibiting IRF-7 limited neutrophil and macrophage influx and IFN responses in nonallergic mice. Neutralizing CCL7 also reduced activation of NF-¿B p65 and p50 subunits, as well as airway hyperreactivity (AHR) in nonallergic mice. However, neither NF-¿B subunit activation nor AHR was abolished with infection of allergic mice after neutralizing CCL7, despite a reduction in the number of neutrophils, macrophages, and eosinophils. IRF-7 small interfering RNA primarily suppressed IFN-a and IFN-b levels during infection of allergic mice. Our data highlight a pivotal role of CCL7 and IRF-7 in RV-induced inflammation and IFN responses and link NF-¿B signaling to the development of AHR.

DOI 10.4049/jimmunol.1401362
Citations Scopus - 27Web of Science - 29
Co-authors Nathan Bartlett, Adam Collison, Joerg Mattes, Paul Foster
2014 Hatchwell L, Girkin J, Morten M, Collison A, Mattes J, Foster PS, et al., 'Salmeterol attenuates chemotactic responses in rhinovirus-induced exacerbation of allergic airways disease by modulating protein phosphatase 2A', Journal of Allergy and Clinical Immunology, (2014) [C1]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning... [more]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning mechanisms remain poorly understood. Recently, a direct interaction between formoterol and protein phosphatase 2A (PP2A) has been described in¿vitro. Objective: We sought to elucidate the molecular mechanisms by which ß-agonists exert anti-inflammatory effects in allergen-driven and rhinovirus 1B-exacerbated allergic airways disease (AAD). Methods: Mice were sensitized and then challenged with house dust mite to induce AAD while receiving treatment with salmeterol, formoterol, or salbutamol. Mice were also infected with rhinovirus 1B to exacerbate lung inflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (S)-2-amino-4-(4-[heptyloxy]phenyl)-2-methylbutan-1-ol (AAL[S]). Results: Systemic or intranasal administration of salmeterol protected against the development of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitment to the lungs as effectively as dexamethasone. Formoterol and salbutamol also showed anti-inflammatory properties. Salmeterol, but not dexamethasone, increased PP2A activity, which reduced CCL11, CCL20, and CXCL2 expression and reduced levels of phosphorylated extracellular signal-regulated kinase 1 and active nuclear factor ¿B subunits in the lungs. The anti-inflammatory effect of salmeterol was blocked by targeting the catalytic subunit of PP2A with small RNA interference. Conversely, increasing PP2A activity with AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CCL20, and CXCL2 expression. Salmeterol also directly activated immunoprecipitated PP2A in¿vitro isolated from human airway epithelial cells. Conclusions: Salmeterol exerts anti-inflammatory effects by increasing PP2A activity in AAD and rhinovirus-induced lung inflammation, which might potentially account for some of its clinical benefits. © 2013 American Academy of Allergy, Asthma & Immunology.

DOI 10.1016/j.jaci.2013.11.014
Citations Scopus - 28Web of Science - 27
Co-authors Joerg Mattes, Nikki Verrills, Adam Collison, Matt Dun, Paul Foster
Show 6 more journal articles

Conference (7 outputs)

Year Citation Altmetrics Link
2019 Williams T, Girkin J, Nichol K, Knight D, Alton K, Shimkets R, Bartlett N, 'IL-25 BLOCKADE AUGMENTS EPITHELIAL ANTIVIRAL IMMUNITY DURING RHINOVIRUS INFECTION', RESPIROLOGY (2019)
Co-authors Nathan Bartlett
2018 Bartlett N, Girkin J, Williams T, Vincent T, Jackson C, Alton K, Shimkets R, 'ABM125 Anti-IL-25 Antibody Pre-Clinical Development for Viral Asthma Exacerbations Identifies IL-25 Mediated Regulation of Type-2-and Anti-Viral Immunity', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Citations Web of Science - 1
Co-authors Nathan Bartlett
2018 Bartlett NW, Girkin J, Wong C, Deliyannis G, Zeng W, Demaison C, Jackson DC, 'Upper Airway TLR2 Immune Modulators Prime Broad Respiratory Immunity Against Rhinovirus and Influenza Infection and Inhibit Subsequent Lung Inflammation', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Co-authors Nathan Bartlett
2014 Collison A, Hatchwell L, Girkin J, Parsons K, Li J, Zhang J, et al., 'Late-breaking abstract: IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression may impair the interferon response to rhinovirus in allergic airways', EUROPEAN RESPIRATORY JOURNAL (2014)
Co-authors Adam Collison, Nathan Bartlett, Paul Foster, Joerg Mattes, Peter Wark
2014 Collison A, Hatchwell L, Girkin J, Li J, Parsons K, Bartlett N, et al., 'REDUCED TLR7 EXPRESSION MAY UNDERPIN IMPAIRED RESPONSE TO VIRAL INFECTION IN ASTHMA', RESPIROLOGY (2014) [E3]
DOI 10.1111/resp.12263_5
Co-authors Paul Foster, Joerg Mattes, Adam Collison, Peter Wark
2014 Girkin J, Sokulsky L, Hatchwell L, Starkey M, Collison A, Hansbro P, Mattes J, 'IDENTIFICATION OF A NOVEL INTERLEUKIN-13 SIGNALLING PATHWAY', RESPIROLOGY (2014) [E3]
Co-authors Adam Collison, Malcolm Starkey, Joerg Mattes, Philip Hansbro
2013 Girkin J, Hatchwell L, Foster PS, Johnston SL, Collison A, Mattes J, 'SALMETEROL ATTENUATES CHEMOTAXIS IN RHINOVIRUS-INDUCED EXACERBATION OF ASTHMA VIA MODULATION OF PP2A', RESPIROLOGY (2013) [E3]
Co-authors Adam Collison, Joerg Mattes, Paul Foster
Show 4 more conferences
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Grants and Funding

Summary

Number of grants 4
Total funding $65,596

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


20212 grants / $19,726

Repurposing lactoferrin to treat coronavirus infection $14,878

Anti-virals are going to play a key role in containment of COVID-19 as well as treatment for the many current and future respiratory viral diseases. Lactoferrin is a multifunctional, innate immune glycoprotein present in a range of secretory fluids including milk, saliva, tears and nasal secretions. Purified bovine lactoferrin is widely used as a dietary supplement. Studies in vitro (in cell lines) have reported the anti-viral activity of lactoferrin for a range of respiratory viruses, including SARS-CoV-2). CI Esneau and CI Bartlett have extended these results by demonstrating the antiviral properties of lactoferrin (PUREnFERRIN, produced by Australian company Freedom Foods) –in differentiated primary human bronchial epithelial cells infected with endemic human coronaviruses (eg OC43) as well as SARS-CoV2.

Here we aim to generate proof of concept in vivo antiviral efficacy data to support development of inhaled lactoferrin treatment using a novel laboratory model of OC43 respiratory infection developed by CI Girkin.

Funding body: College of Health, Medicine and Wellbeing, University of Newcastle

Funding body College of Health, Medicine and Wellbeing, University of Newcastle
Project Team

CIA: Jason Girkin, CIB: Camille Esneau

Scheme Strategic Research Pilot Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo
Type Of Funding Internal
Category INTE
UON N

Pilot funding to investigate the role of adipocytes on suppressed antiviral responses of the respiratory epithelium$4,848

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Jason Girkin
Scheme Research Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo G2100116
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

20201 grants / $4,870

Mycoplasma screening lab$4,870

  • One of the most problematic issues effecting cell culture is mycoplasma contamination and unlike bacterial and fungal contamination, mycoplasma is not easily detected. Mycoplasma contamination in a single culture can quickly spread, effecting the physiology, metabolism and immunological responses of the cells grown in an entire laboratory space.
  • A minor facility restructure has allowed for a dedicated screening lab for mycoplasma (deemed ‘Dirty tissue culture lab’), eliminating contamination in all cell culture systems used by the respiratory medicine and immunology groups working at HMRI in the clean, viral and bacterial labs.
  • This facility is currently insufficiently equipped and we are requesting basic pipetting and media warming equipment that is required to meet the increasing demands for mycoplasma screening with recent (and forecasted) increases in the volume and diversity of cell culture systems originating in the mycoplasma screening lab.
  • Requested equipment includes pipettes, serological pipettes and steel beads used for media warming to replace water baths (a potential source of contamination):

Funding body: School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

Funding body School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Project Team

CIA: Jason Girkin

Scheme 2020 SBSP Equipment Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

20191 grants / $41,000

QiaAgility automated liquid handling station$41,000

This equipment contains an air handling HEPA filtration unit and UV decontamination measures to prevent contamination of sensitive qPCR reactions. The automated workflow frees up time otherwise spent on manually setting up qPCR plates. Robotic precision standardised qPCR workflow and increased accuracy and precision of qPCR data.
This equipment funding supported research groups funded by NHMRC funding,  Australian Cystic Fibrosis Research Trust, NSW Ministry of Health, Industry collaborations (including  Sanofi, GlaxoSmithKline, AstraZeneca, Abeome, Ena Respiratory and various forms of Trust funding.

Funding body: Faculty of Health and Medicine Research Equipment Grant Round

Funding body Faculty of Health and Medicine Research Equipment Grant Round
Project Team

CIA: Jason Girkin

Scheme Faculty of Health and Medicine Research Equipment Grant Round
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N
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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 17
United Kingdom 9
China 2
United States 2
Japan 1
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Dr Jason Girkin

Positions

Associate Lecturer
Viral Immunology and Respiratory Disease, Priority Research Centre for Healthy Lungs
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

Casual Lecturer
Viral Immunology and Respiratory Disease, Priority Research Centre for Healthy Lungs
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

Contact Details

Email jason.girkin@newcastle.edu.au
Phone (02) 40420847
Links Twitter
Research Networks

Office

Building HMRI -Hunter Medical Research Institute
Location Hunter Medical Research Institute

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