Ms Sharron Hall

Research Coordinator

School of Medicine and Public Health (Immunology and Microbiology)

Career Summary

Biography

Research Expertise
Management of research projects relating to the immunology of the upper respiratory tract, particularly immune fucntion in elite athletes, infants at risk of sudden infant death and children with otitis media with effusion. Use of saliva for studies of mucosal immune function. Studies in the pathology of Aboriginal Health. Development of enzyme-linked immuno assays. Ethics and safety applications. training new staff.

Administrative Expertise
Management of research funds.

Qualifications

  • Bachelor of Science, University of Newcastle

Keywords

  • mucosal immunology

Fields of Research

Code Description Percentage
110799 Immunology not elsewhere classified 50
110899 Medical Microbiology not elsewhere classified 50

Professional Experience

Professional appointment

Dates Title Organisation / Department
1/01/1983 -  Hospital Scientist Hunter New England Health
Hunter Area Pathology Service, Immunology Department
Australia
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (24 outputs)

Year Citation Altmetrics Link
2015 Moscovis SM, Gordon AE, Al Madani OM, Gleeson M, Scott RJ, Hall ST, et al., 'Genetic and environmental factors affecting TNF-a responses in relation to sudden infant death syndrome', Frontiers in Immunology, 6 (2015) [C1]

© 2015 Moscovis, Gordon, Al Madani, Gleeson, Scott, Hall, Burns and Blackwell. Dysregulation of the inflammatory responses has been suggested to contribute to the events leading ... [more]

© 2015 Moscovis, Gordon, Al Madani, Gleeson, Scott, Hall, Burns and Blackwell. Dysregulation of the inflammatory responses has been suggested to contribute to the events leading to sudden infant deaths. Our objectives were (1) to analyze a single nucleotide polymorphism (SNP) associated with high levels of tumor necrosis factor-a (TNF-a) responses, TNF G-308A, in sudden infant death syndrome (SIDS) infants, SIDS and control parents, and ethnic groups with different incidences of SIDS; (2) the effects of two risk factors for SIDS, cigarette smoke and virus infection, on TNF-a responses; and (3) to assess effects of genotype, cigarette smoke, and gender on TNF-a responses to bacterial toxins identified in SIDS infants. TNF G-308A genotypes were determined by real-time polymerase chain reaction for SIDS infants from Australia, Germany, and Hungary; parents of SIDS infants and their controls; and populations with high (Aboriginal Australian), medium (Caucasian), and low (Bangladeshi) SIDS incidences. Leukocytes from Caucasian donors were stimulated in vitro with endotoxin or toxic shock syndrome toxin-1 (TSST-1). TNF-a responses were measured by L929 bioassay (IU/ml) and assessed in relation to genotype, smoking status, and gender. There was a significantly higher proportion of the minor allele AA genotype among Australian SIDS infants (6/24, 24%) compared to 3/62 (4.8%) controls (p = 0.03). There were no significant differences in TNF-a responses by TNF G-308A genotypes when assessed in relation to smoking status or gender. Given the rarity of the TNF G-308A A allele in Caucasian populations, the finding that 24% of the Australian SIDS infants tested had this genotype requires further investigation and cautious interpretation. Although non-smokers with the AA genotype had higher TNFa responses to both TSST-1 and endotoxin, there were too few subjects with this rare allele to obtain statistically valid results. No effects of genotype, smoking, or gender were observed for TNF-a responses to these toxins.

DOI 10.3389/fimmu.2015.00374
Co-authors Caroline Blackwell, Maree Gleeson, Rodney Scott
2015 Moscovis SM, Cox A, Hall ST, Burns CJ, Scott RJ, Blackwell CC, 'Effects of gender, cytokine gene polymorphisms and environmental factors on inflammatory responses', Innate Immunity, 21 523-530 (2015) [C1]

© The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav. Previous studies have indicated that cytokine gene polymorphisms of Indigenous Australians w... [more]

© The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav. Previous studies have indicated that cytokine gene polymorphisms of Indigenous Australians were predominantly associated with strong pro-inflammatory responses. We tested the hypothesis that cells of donors with genetic profiles of inflammatory cytokine single nucleotide polymorphisms (SNPs) similar to Indigenous Australians produce higher pro-inflammatory responses. PBMCs from 14 donors with genetic profiles for a high risk of strong pro-inflammatory responses and 14 with low-risk profiles were stimulated with endotoxin and effects of gender, IFN-¿, cigarette smoke extract (CSE) and testosterone on cytokine responses analysed. Cytokines were calculated from standard curves (Luminex 2.3 software). No significant differences were associated with SNP profile alone. Lower pro-inflammatory responses were observed for cells from males with low- or high-risk profiles. For cells from females with high-risk profiles, anti-inflammatory IL-10 responses were significantly reduced. There was no effect of testosterone levels on responses from males. For females, results from IFN-¿-treated cells showed positive correlations between testosterone levels and IL-1ß responses to endotoxin for both risk groups and TNF-a for the high-risk group. If interactions observed among CSE, IFN-¿, genetic background and testosterone reflect those in vivo, these might contribute to increased incidences of hospitalisations for infectious diseases among Indigenous women.

DOI 10.1177/1753425914553645
Citations Scopus - 2Web of Science - 1
Co-authors Caroline Blackwell, Rodney Scott
2015 Pringle KG, Rae K, Weatherall L, Hall S, Burns C, Smith R, et al., 'Effects of maternal inflammation and exposure to cigarette smoke on birth weight and delivery of preterm babies in a cohort of Indigenous Australian women', Frontiers in Immunology, 6 (2015) [C1]

© 2015 Pringle, Rae, Weatherall, Hall, Burns, Smith, Lumbers and Blackwell. Sudden infant death syndrome (SIDS), neonatal deaths, and deaths from infection are higher among Indig... [more]

© 2015 Pringle, Rae, Weatherall, Hall, Burns, Smith, Lumbers and Blackwell. Sudden infant death syndrome (SIDS), neonatal deaths, and deaths from infection are higher among Indigenous Australians. This study aimed to determine the effects of inflammatory responses and exposure to cigarette smoke, two important factors associated with sudden death in infancy, on preterm birth, and birth weight in a cohort of Indigenous mothers. Indigenous Australian women (n = 131) were recruited as part of a longitudinal study while attending antenatal care clinics during pregnancy; blood samples were collected up to three times in pregnancy. Serum cotinine, indicating exposure to cigarette smoke, was detected in 50.4% of mothers. Compared with non-Indigenous women, the cohort had 10 times the prevalence of antibodies to Helicobacter pylori (33 vs. 3%). Levels of immunoglobulin G, antibodies to H. pylori, and C-reactive protein (CRP) were all inversely correlated with gestational age (P < 0.05). CRP levels were positively associated with maternal body mass index (BMI; ¿ = 0.449, P = 0.001). The effects of cigarette smoke (cotinine) and inflammation (CRP) were assessed in relation to risk factors for SIDS: gestational age at delivery and birth weight. Serum cotinine levels were negatively associated with birth weight (¿ = -0.37, P < 0.001), this correlation held true for both male (¿ = -0.39, P = 0.002) and female (¿ = -0.30, P = 0.017) infants. Cotinine was negatively associated with gestational age at delivery (¿ = -0.199, P = 0.023). When assessed by fetal sex, this was significant only for males (¿ = -0.327, P = 0.011). CRP was negatively associated with gestational age at delivery for female infants (¿ = -0.46, P < 0.001). In contrast, maternal BMI was significantly correlated with birth weight. These data highlight the importance of putting programs in place to reduce cigarette smoke exposure in pregnancy and to treat women with chronic infections such as H. pylori to improve pregnancy outcomes and decrease risk factors for sudden death in infancy.

DOI 10.3389/fimmu.2015.00089
Co-authors Caroline Blackwell, Roger Smith, Kirsty Pringle, Kym Rae
2015 Blackwell C, Moscovis S, Hall S, Burns C, Scott RJ, 'Exploring the risk factors for sudden infant deaths and their role in inflammatory responses to infection', Frontiers in Immunology, 6 (2015) [C1]

© 2015 Blackwell, Moscovis, Hall, Burns and Scott. The risk factors for sudden infant death syndrome (SIDS) parallel those associated with susceptibility to or severity of infect... [more]

© 2015 Blackwell, Moscovis, Hall, Burns and Scott. The risk factors for sudden infant death syndrome (SIDS) parallel those associated with susceptibility to or severity of infectious diseases. There is no evidence that a single infectious agent is associated with SIDS; the common thread appears to be induction of inflammatory responses to infections. In this review, interactions between genetic and environmental risk factors for SIDS are assessed in relation to the hypothesis that many infant deaths result from dysregulation of inflammatory responses to "minor" infections. Risk factors are assessed in relation to three important stages of infection: (1) bacterial colonization (frequency or density); (2) induction of temperature-dependent toxins; (3) induction or control of inflammatory responses. In this article, we review the interactions among risk factors for SIDS for their effects on induction or control of inflammatory responses. The risk factors studied are genetic factors (sex, cytokine gene polymorphisms among ethnic groups at high or low risk of SIDS); developmental stage (changes in cortisol and testosterone levels associated with 2- to 4-month age range); environmental factors (virus infection, exposure to cigarette smoke). These interactions help to explain differences in the incidences of SIDS observed between ethnic groups prior to public health campaigns to reduce these infant deaths.

DOI 10.3389/fimmu.2015.00044
Co-authors Rodney Scott, Caroline Blackwell
2015 Burns C, Hall ST, Smith R, Blackwell C, 'Cytokine levels in late pregnancy: Are female infants better protected against inflammation?', Frontiers in Immunology, 6 (2015) [C1]

© 2015 Burns, Hall, Smith and Blackwell. Inflammatory responses have been implicated in several forms of infant deaths (sudden expected deaths and stillbirths) and the initiation... [more]

© 2015 Burns, Hall, Smith and Blackwell. Inflammatory responses have been implicated in several forms of infant deaths (sudden expected deaths and stillbirths) and the initiation of pre-term births. In this study, we examined matched samples of term maternal blood, cord blood, and amniotic fluid obtained from 24 elective cesarean deliveries for both pro- and anti-inflammatory cytokines thought to be important in maintaining a balanced response leading to successful pregnancy outcome. These included interleukin (IL)-1ß, IL-6, IL-8, tumor necrosis factor-a (TNF-a), interferon-¿ (IFN-¿), IL-10, and IL-1 receptor antagonist (IL-1ra). Amniotic fluid levels for each of the cytokines examined were significantly higher than those for cord blood or maternal plasma. While pro-inflammatory cytokines were higher in amniotic fluid associated with male fetuses compared with females, the major significant difference was higher levels of IL-1ra in amniotic fluid associated with female fetuses. Our study supports similar findings for cytokines during mid-trimester, which noted that amniotic fluid levels were higher than those in maternal blood. Our study suggests that maternal decidua secretes additional IL-ra in the presence of a female conceptus which improves the likelihood of a good outcome compared to pregnancies with male fetuses.

DOI 10.3389/fimmu.2015.00318
Citations Scopus - 1Web of Science - 1
Co-authors Caroline Blackwell, Roger Smith
2015 Moscovis SM, Gordon AE, Al Madani OM, Gleeson M, Scott RJ, Hall ST, et al., 'Virus infections and sudden death in infancy: The role of interferon-¿', Frontiers in Immunology, 6 (2015) [C1]

© 2015 Moscovis, Gordon, Al Madani, Gleeson, Scott, Hall, Burns and Blackwell. Respiratory infections have been implicated in sudden infant death syndrome (SIDS). As interferon-Â... [more]

© 2015 Moscovis, Gordon, Al Madani, Gleeson, Scott, Hall, Burns and Blackwell. Respiratory infections have been implicated in sudden infant death syndrome (SIDS). As interferon-¿ (IFN-¿) is a major response to virus infection, we examined (1) the frequency of single nucleotide polymorphism (SNP), IFNG T + 874A, in SIDS infants, their parents, and ethnic groups with different incidences of SIDS; (2) model systems with a monocytic cell line (THP-1) and human peripheral blood monocytes (PBMC) for effects of levels of IFN-¿ on inflammatory responses to bacterial antigens identified in SIDS; (3) interactions between genetic and environmental factors on IFN-¿ responses. IFNG T + 874A genotypes were determined for SIDS infants from three countries; families who had a SIDS death; populations with high (Indigenous Australian), medium (Caucasian), and low (Bangladeshi) SIDS incidences. The effect of IFN-¿ on cytokine responses to endotoxin was examined in model systems with THP-1 cells and human PBMC. The IFN-¿ responses to endotoxin and toxic shock syndrome toxin (TSST-1) were assessed in relation to genotype, gender, and reported smoking. There was a marginal association with IFNG T + 874A genotype and SIDS (p = 0.06). Indigenous Australians had significantly higher proportions of the IFNG T + 874A SNP (TT) associated with high responses of IFN-¿. THP-1 cells showed a dose dependent effect of IFN-¿ on cytokine responses to endotoxin. For PBMC, IFN-¿ enhanced interleukin (IL)-1ß, IL-6, and tumor necrosis factor-a responses but reduced IL-8 and IL-10 responses. Active smoking had a suppressive effect on baseline levels of IFN-¿. There was no effect of gender or genotype on IFN-¿ responses to bacterial antigens tested; however, significant differences were observed between genotypes in relation to smoking. The results indicate virus infections contribute to dysregulation of cytokine responses to bacterial antigens and studies on physiological effects of genetic factors must include controls for recent or concurrent infection and exposure to cigarette smoke.

DOI 10.3389/fimmu.2015.00107
Citations Scopus - 1Web of Science - 1
Co-authors Rodney Scott, Maree Gleeson, Caroline Blackwell
2014 Moscovis S, Hall S, Burns C, Scott R, Blackwell C, 'Development of an experimental model for assessing the effects of cigarette smoke and virus infections on inflammatory responses to bacterial antigens', Innate Immunity, 20 647-658 (2014) [C1]

Interactions among major risk factors associated with bacterial infections were assessed in a model system using surrogates for virus infection; IFN-g, and exposure to cigarette s... [more]

Interactions among major risk factors associated with bacterial infections were assessed in a model system using surrogates for virus infection; IFN-g, and exposure to cigarette smoke; cigarette smoke extract (CSE), nicotine and cotinine. Cytokine responses elicited by LPS from THP-1 cells in the presence of these components, or combinations of components, were assessed by multiplex bead assay, i.e. IL-1ß, IL-6, IL-8, IL-10, TNF-a and IFN-¿. IFN-¿-priming significantly increased pro-inflammatory cytokines induced by LPS. CSE suppressed production of pro-inflammatory cytokines IL-1ß, TNF-a and IFN-¿, but enhanced production of IL-8. Nicotine and cotinine suppressed all cytokine responses. In combination, IFN-¿ masked the inhibitory effects of CSE. In relation to the objectives of the study, we concluded that (a) IFN¿ at biologically relevant concentrations significantly enhanced pro-inflammatory responses; (b) CSE, nicotine and cotinine dysregulated the inflammatory response and that the effects of CSE were different from those of the individual components, nicotine and cotinine; (c) when both IFN-¿ and CSE were present, IFN-¿ masked the effect of CSE. There is a need for clinical investigations on the increase in IL-8 responses in relation to exposure to cigarette smoke and increased pro-inflammatory responses in relation to recent viral infection. © 2013 The Author(s).

DOI 10.1177/1753425913503893
Citations Scopus - 6Web of Science - 6
Co-authors Rodney Scott, Caroline Blackwell
2014 Campbell V, Anstey C, Gray NA, Jones D, Hall S, Parke R, Mcguinness S, 'MIDKINE LEVELS IN ACUTE KIDNEY INJURY AFTER CARDIAC BYPASS', NEPHROLOGY, 19 48-48 (2014)
2014 Campbell V, Gray NA, Anstey C, Gately R, Clark C, Noble E, et al., 'MIDKINE LEVELS IN PEOPLE WITH CHRONIC KIDNEY DISEASE', NEPHROLOGY, 19 60-60 (2014)
2014 Campbell V, Gray NA, Anstey C, Gately R, Clark C, Noble E, et al., 'MIDKINE LEVELS CAN BE MEASURED IN EITHER PLASMA OR SERUM', NEPHROLOGY, 19 60-60 (2014)
2014 Moscovis SM, Hall ST, Burns CJ, Scott RJ, Blackwell CC, 'The male excess in sudden infant deaths', INNATE IMMUNITY, 20 24-29 (2014) [C1]
DOI 10.1177/1753425913481071
Citations Scopus - 9Web of Science - 9
Co-authors Caroline Blackwell, Rodney Scott
2014 Ashhurst-Smith C, Hall ST, Burns CJ, Stuart J, Blackwell CC, 'Induction of inflammatory responses from THP-1 cells by cell-free filtrates from clinical isolates of Alloiococcus otitidis', INNATE IMMUNITY, 20 283-289 (2014) [C1]
DOI 10.1177/1753425913490535
Co-authors John Stuart, Caroline Blackwell
2014 Ashhurst-Smith C, Hall ST, Burns CJ, Stuart J, Blackwell CC, 'Invitro inflammatory responses elicited by isolates of Alloiococcus otitidis obtained from children with otitis media with effusion', INNATE IMMUNITY, 20 320-326 (2014) [C1]
DOI 10.1177/1753425913492181
Citations Scopus - 1Web of Science - 1
Co-authors John Stuart, Caroline Blackwell
2013 Titmarsh CJ, Moscovis SM, Hall S, Tzanakaki G, Kesanopoulos K, Xirogianni A, et al., 'Comparison of cytokine gene polymorphisms among Greek patients with invasive meningococcal disease or viral meningitis', JOURNAL OF MEDICAL MICROBIOLOGY, 62 694-700 (2013) [C1]
DOI 10.1099/jmm.0.058073-0
Citations Scopus - 2Web of Science - 3
Co-authors Caroline Blackwell, Rodney Scott
2012 Ashhurst-Smith CIJ, Hall ST, Stuart J, Burns CJ, Liet E, Walker PJ, et al., 'Alloiococcus otitidis: An emerging pathogen in otitis media', Journal of Infection, 64 233-235 (2012) [C1]
Citations Scopus - 5Web of Science - 4
Co-authors Caroline Blackwell, John Stuart
2007 Ashhurst-Smith CIJ, Hall ST, Walker PJ, Stuart JE, Hansbro PM, Blackwell CC, 'Isolation of Alloiococcus otitidis from Indigenous and non-Indigenous Australian children with chronic otitis media with effusion', FEMS Immunology and Medical Microbiology, 51 163-170 (2007) [C1]
DOI 10.1111/j.1574-695X.2007.00297.x
Citations Scopus - 22Web of Science - 18
Co-authors Caroline Blackwell, Philip Hansbro, John Stuart
2006 Moscovis SM, Gordon AE, Al Madani OM, Gleeson M, Scott R, Roberts-Thomson JM, et al., 'IL6 G-174C Associated With Sudden Infant Death Syndrome in a Caucasian Australian Cohort', Human Immunology, 67 819-825 (2006) [C1]
DOI 10.1016/j.humimm.2006.07.010
Citations Scopus - 32Web of Science - 32
Co-authors Caroline Blackwell, Maree Gleeson, Rodney Scott
2005 Blackwell CC, Moscovis SM, Gordon AE, Al Madani OM, Hall S, Gleeson M, et al., 'Cytokine responses and sudden infant death: genetic, developmental, and environmental risk factors', Journal of Leukocyte Biology, 78 1242-1254 (2005) [C1]
DOI 10.1189/jlb.0505253
Citations Scopus - 57Web of Science - 52
Co-authors Rodney Scott, Maree Gleeson, Caroline Blackwell
2004 Gleeson M, Clancy RL, Cox AJ, Gulliver SA, Hall ST, Cooper DM, 'Mucosal immune responses to infections in infants with acute life threatening events classified as 'near-miss' sudden infant death syndorme', FEMS Immunology and Medical Microbiology, 42 105-118 (2004) [C1]
DOI 10.1016/j.femsim.2004.06.019
Citations Scopus - 15Web of Science - 8
Co-authors Maree Gleeson
2004 Moscovis SM, Gordon AE, Al Madani OM, Gleeson M, Scott R, Roberts-Thomson JM, et al., 'Interleukin-10 and sudden infant death syndrome', FEMS Immunology and Medical Microbiology, 42 130-138 (2004) [C1]
DOI 10.1016/j.femsim.2004.06.020
Citations Scopus - 35Web of Science - 33
Co-authors Maree Gleeson, Caroline Blackwell, Rodney Scott
2004 Moscovis SM, Gordon AE, Hall ST, Gleeson M, Scott R, Roberts-Thomson JM, et al., 'Interleukin 1-b responses to bacterial toxins and sudden infant death syndrome', FEMS Immunology and Medical Microbiology, 42 139-145 (2004) [C1]
DOI 10.1016/j.femsim.2004.06.005
Citations Scopus - 27Web of Science - 25
Co-authors Maree Gleeson, Caroline Blackwell, Rodney Scott
2004 Blackwell CC, Moscovis SM, Gordon AE, Al Madani OM, Hall ST, Gleeson M, et al., 'Ethnicity, infection and sudden infant death syndrome', FEMS Immunology and Medical Microbiology, 42 53-65 (2004) [C1]
DOI 10.1016/j.femsim.2004.06.007
Citations Scopus - 31Web of Science - 21
Co-authors Maree Gleeson, Rodney Scott, Caroline Blackwell
2000 Reeves GE, Burns C, Hall ST, Gleeson M, Lemmert K, Clancy RL, 'The measurement of IgA and IgG transglutaminase antibodies in celiac disease: a comparison with current diagnostic methods', Pathology, 32 181-185 (2000) [C1]
Citations Scopus - 26Web of Science - 24
Co-authors Maree Gleeson
1999 Gleeson M, Hall S, McDonald W, Flanagan A, Clancy RL, 'Salivary IgA subclasses and infection risk in elite swimmers', Immunology & Cell Biology, 77 351-355 (1999) [C1]
Citations Scopus - 50Web of Science - 41
Co-authors Maree Gleeson
Show 21 more journal articles

Conference (9 outputs)

Year Citation Altmetrics Link
2015 Zdenkowski N, Plowman L, Hall S, Jones D, Ackland S, 'MIDKINE (MK) AS A PREDICTIVE BIOMARKER IN METASTATIC COLORECTAL CANCER (mCRC)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Stephen Ackland
2014 Pringle K, Rae KM, Weatherall L, Hall S, Burns C, Smith R, et al., 'Effects of cigarette smoke and maternal inflammation in pregnancy on birth weight and gestational age at delivery in an Indigenous Australian population', Proceedings of the 57th ESA and 45th SRB Annual Conference (2014) [E3]
Co-authors Kym Rae, Kirsty Pringle, Roger Smith, Caroline Blackwell
2014 Ackland SP, Zdenkowski N, Adler K, Hall S, Jones D, 'MIDKINE AS A PREDICTIVE MARKER IN METASTATIC COLORECTAL CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Stephen Ackland
2013 Rae KM, Weatherall L, Clausen D, Maxwell C, Bowman M, Milgate P, et al., 'Gomeroi gaaynggal: Empowerment of Aboriginal communities to understand health implications of research in pregnancy', Proceedings of th 12th National Rural Health Conference (2013) [E1]
Co-authors Roger Smith, Maria Bowman, Kym Rae
2011 Weatherall LJ, Rae KM, Milgate P, Hall ST, Carlin A, Boyd J, et al., 'A place of connections: The Gomeroi Gaaynggal Centre', Proceedings of the 3rd Coalition for Research to Improve Aboriginal Health (CRIAH) Aboriginal Health Research Conference (2011) [E3]
Co-authors Roger Smith, Maria Bowman, Kym Rae
2011 Moscovis SM, Hall ST, Gleeson M, Scott R, Blackwell CC, 'Genetics, gender and environment: Effects on inflammatory responses and implications for Indigenous women', Proceedings of the 3rd Coalition for Research to Improve Aboriginal Health (CRIAH) Aboriginal Health Research Conference (2011) [E3]
Co-authors Caroline Blackwell, Maree Gleeson, Rodney Scott
2011 Ashhurst-Smith CIJ, Hall ST, Stuart JE, Liet E, Walker PJ, Dorrington R, et al., 'Alloiococcus otitidis: The major isolate from both urban and rural/remote children with chronic otitis media with effusion (glue ear)', Proceedings of the 3rd Coalition for Research to Improve Aboriginal Health (CRIAH) Aboriginal Health Research Conference (2011) [E3]
Co-authors Caroline Blackwell, John Stuart
2011 Ashhurst-Smith CIJ, Hall ST, Stuart JE, Walker PJ, Dorrington R, Eisenberg R, et al., 'Antibiotic resistance among alloiococcus otitidis isolates from Indigenous and non-Indigenous children with otitis media with effusion (OME)', Proceedings of the 3rd Coalition for Research to Improve Aboriginal Health (CRIAH) Aboriginal Health Research Conference (2011) [E3]
Co-authors John Stuart, Caroline Blackwell
2009 Hall ST, Tzanakaki G, Kremastinou J, Scott R, Blackwell CC, Titmarsh CJ, Moscovis SM, 'Comparison of cytokine gene polymorphisms among Greek patients with meningococcal or viral meningitis', The Pediatric Infectious Disease Journal (2009) [E3]
DOI 10.1097/inf.0b013e3181a51c24
Co-authors Caroline Blackwell, Rodney Scott
Show 6 more conferences
Edit

Ms Sharron Hall

Positions

Research Coordinator
School of Medicine and Public Health
Faculty of Health and Medicine

Research Assistant
School of Medicine and Public Health
Faculty of Health and Medicine

Focus area

Immunology and Microbiology

Contact Details

Email sharron.hall@newcastle.edu.au
Phone (02) 40420000
Mobile 0421704761

Office

Room HMRI 3309
Building HMRI building
Location John Hunter Hospital

,
Edit