Dr Hannah Palliser

Dr Hannah Palliser

Research Fellow

School of Biomedical Sciences and Pharmacy (Pharmacy and Experimental Pharmacology)

Career Summary

Biography

Research Expertise
- Premature labour - Intrauterine growth restriction - Fetal and neonatal neurodevelopment and wellbeing - Animal models - Myometrial activity - Progesterone and neuroprotection 

Collaborations
Premature labour, Intrauterine growth restriction, Fetal and neonatal neurodevelopment and wellbeing, Animal models, Myometrial activity, Progesterone and neuroprotection.

Qualifications

  • Doctor of Philosophy, Monash University
  • Bachelor of Science (Biomedical), Monash University
  • Bachelor of Science (Honours)(Biomedical), Monash University

Keywords

  • Fetal
  • Labour
  • Myometrial
  • Neurosciences
  • Paediatrics
  • Reproductive Medicine

Fields of Research

Code Description Percentage
111499 Paediatrics and Reproductive Medicine not elsewhere classified 65
111799 Public Health and Health Services not elsewhere classified 20
170299 Cognitive Sciences not elsewhere classified 15

Professional Experience

UON Appointment

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

Academic appointment

Dates Title Organisation / Department
1/07/2007 - 1/07/2012 Fellow UON

UoN Research Fellowship

University of Newcastle
School of Biomedical Sciences and Pharmacy
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For publications that are currently unpublished or in-press, details are shown in italics.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
2016 Palliser HK, Bennett GA, Kelleher MA, Cumberland AL, Walker DW, Hirst JJ, 'Models of perinatal compromises in the guinea pig: Their use in showing the role of neurosteroids in pregnancy and the newborn', Neuromethods 221-243 (2016)

© Springer Science+Business Media New York 2016.Placental progesterone production during late gestation has a major role in maintaining elevated neurosteroid levels during pregna... [more]

© Springer Science+Business Media New York 2016.Placental progesterone production during late gestation has a major role in maintaining elevated neurosteroid levels during pregnancy. These levels of key neurosteroids, including allopregnanolone, are critical for optimal brain development during late gestation and the early neonatal period. The long gestation period (~70), in utero brain development and placental progesterone synthesis of the guineas pig makes this species very suitable for studying the mechanisms by which pregnancy compromises impact neurosteroid pathways. We have used models of intrauterine growth restriction and preterm birth to show that these challenges may suppress neurosteroid action and this likely contributes to the adverse outcomes following these conditions. Reduced allopregnanolone levels during late gestation result in reduced myelination and injurious brain cell death suggesting supplementation treatments may improve outcomes following compromised pregnancy. Guinea pig models of episodic prenatal maternal stress have been used to examine how these events lead to adverse behavioral outcomes for the offspring. We found that prenatal stress disrupts the neurosteroid pathways between the dam and fetus. Together this work indicates that compromises and stress during pregnancy and in the early neonatal period disrupt neurotropic and protective neurosteroid pathways leading to deficiencies that contribute to the adverse neurological and behavioral outcomes following these challenges. The use of neurosteroid-based supplementation therapies may represent a future range of therapeutic approaches that could be used to improve outcomes following stressful events in pregnancy and following premature birth.

DOI 10.1007/978-1-4939-3014-2_11

Journal article (34 outputs)

Year Citation Altmetrics Link
2016 Saif Z, Dyson RM, Palliser HK, Wright IM, Lu N, Clifton VL, 'Identification of Eight Different Isoforms of the Glucocorticoid Receptor in Guinea Pig Placenta: Relationship to Preterm Delivery, Sex and Betamethasone Exposure.', PLoS One, 11 e0148226 (2016)
DOI 10.1371/journal.pone.0148226
Co-authors Ian Wright
2016 Bennett GA, Palliser HK, Walker D, Hirst J, 'Severity and timing: How prenatal stress exposure affects glial developmental, emotional behavioural and plasma neurosteroid responses in guinea pig offspring', Psychoneuroendocrinology, 70 47-57 (2016)

© 2016 Elsevier Ltd.Prenatal stress has been associated with a variety of developmental changes in offspring, notably those associated with brain development and subsequent risk ... [more]

© 2016 Elsevier Ltd.Prenatal stress has been associated with a variety of developmental changes in offspring, notably those associated with brain development and subsequent risk for neuropathologies later in life. Recently, the importance of the timing and the severity of the stressor during pregnancy has been emphasized with neurosteroids including allopregnanolone implicated in the regulation of stress and also for endogenous neuroprotection in offspring.Prenatal stress was induced using strobe light exposure in pregnant guinea pigs (term 71 days) in three defined stress exposure groups (Gestational Age (GA)35-65, GA50-65 and GA60-65). Stress was induced for 2 h (9-11 am) every 5 days via strobe light exposure. A fetal cohort were euthanased at term with fetal brains and plasma collected. Anxiety-like behaviour was evaluated at 18 days of age in a separate cohort of offspring with brains and plasma collected at 21 days of age. Markers for mature oligodendrocytes and reactive astrocytes were measured in the CA1 region of the hippocampus and the subcortical white matter. The neurosteroid allopregnanolone was measured by radioimmunoassay in offspring plasma.In the CA1 region of the hippocampus, fetuses from all stress groups showed reduced expression of mature oligodendrocytes and reactive astrocytes. By juvenility, all male stress exposure groups had recovered to levels of unaffected controls with the exception of the GA35-65 stress group. In juvenile females, mature oligodendrocyte marker expression was reduced in all stress groups and reactive astrocyte expression was reduced in the GA35-65 and GA60-65 stress groups by juvenility. Increased reactive astrocyte expression was also apparent in the subcortical white matter in both sexes both at term and at juvenility. Prenatally stressed offspring spent less time exploring in the object exploration test and also entered the inner zone of the open field less than controls at 18 days of age. Circulating allopregnanolone concentrations were significantly reduced in GA35-65 and GA 60-65 stress exposed fetuses with those in the GA35-65 stress group remaining reduced by juvenility.This study has shown the effects of differing levels of prenatal stress severity and timing on glial development, emotional behaviour and plasma allopregnanolone concentrations in offspring.

DOI 10.1016/j.psyneuen.2016.04.011
Co-authors Jon Hirst
2016 Hirst JJ, Cumberland AL, Shaw JC, Bennett GA, Kelleher MA, Walker DW, Palliser HK, 'Loss of neurosteroid-mediated protection following stress during fetal life.', J Steroid Biochem Mol Biol, 160 181-188 (2016)
DOI 10.1016/j.jsbmb.2015.09.012
Co-authors Jon Hirst
2016 Cumberland AL, Palliser HK, Walker DW, Hirst JJ, 'Cerebellar Changes in Guinea Pig Offspring Following Suppression of Neurosteroid Synthesis During Late Gestation.', Cerebellum, (2016)
DOI 10.1007/s12311-016-0802-0
2016 Shaw JC, Palliser HK, Dyson RM, Hirst JJ, Berry MJ, 'Long-term effects of preterm birth on behavior and neurosteroid sensitivity in the guinea pig.', Pediatr Res, (2016)
DOI 10.1038/pr.2016.63
Co-authors Jon Hirst
2015 Bennett GA, Palliser HK, Shaw JC, Walker D, Hirst JJ, 'Prenatal stress alters hippocampal neuroglia and increases anxiety in childhood', Developmental Neuroscience, 37 533-545 (2015) [C1]

© 2015 S. Karger AG, Basel.Prenatal stress has been associated with detrimental outcomes of pregnancy, including altered brain development leading to behavioural pathologies. The... [more]

© 2015 S. Karger AG, Basel.Prenatal stress has been associated with detrimental outcomes of pregnancy, including altered brain development leading to behavioural pathologies. The neurosteroid allopregnanolone has been implicated in mediating some of these adverse outcomes following prenatal stress due to its potent inhibitory and anxiolytic effects on the brain. The aims of the current study were to characterise key markers for brain development as well as behavioural parameters, adrenocortical responses to handling and possible neurosteroid influences towards outcomes in Guinea pig offspring in childhood. Pregnant Guinea pig dams were exposed to strobe light for 2 h (9-11 a.m.) on gestational days 50, 55, 60, and 65 and were left to deliver spontaneously at term and care for their litter. Behavioural testing (open-field test, object exploration test) of the offspring was performed at postnatal day 18 (with salivary cortisol and DHEA measured), and brains were collected at post-mortem on day 21. Markers of brain development myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were assessed via immunohistochemistry, and the neurosteroid allopregnanolone and its rate-limiting enzymes 5a-reductase types 1 and 2 (5aR1/2) were measured in neonatal brains by radioimmunoassay, reverse transcriptase polymerase chain reaction (RT-PCR), and Western blot, respectively. Brain-derived neurotrophic factor protein was measured as a marker of synaptic plasticity, and GABAA receptor subunit expression was also assessed using RT-PCR. Neonates born from mothers stressed during late pregnancy showed a reduction in both MBP (p < 0.01) and GFAP (p < 0.05) expression in the CA1 region of the hippocampus at 21 days of age. Pups of prenatally stressed pregnancies also showed higher levels of anxiety and neophobic behaviours at the equivalent of childhood (p < 0.05). There were no significant changes observed in allopregnanolone levels, 5aR1/2 expression, or GABAA receptor subunit expression in prenatally stressed neonates compared to controls. This study shows alterations in markers of myelination and reactive astrocytes in the hippocampus of offspring exposed to prenatal stress. These changes are also observed in offspring that show increased anxiety behaviours at the equivalent of childhood, which indicates ongoing structural and functional postnatal changes after prenatal stress exposure.

DOI 10.1159/000437302
Citations Scopus - 1
Co-authors Jon Hirst
2015 Dyson RM, Palliser HK, Latter JL, Kelly MA, Chwatko G, Glowacki R, Wright IMR, 'Interactions of the gasotransmitters contribute to microvascular tone (Dys)regulation in the preterm neonate', PLoS ONE, 10 (2015) [C1]

© 2015 Dyson et al.Background & Aims: Hydrogen sulphide (H2S), nitric oxide (NO), and carbon monoxide (CO) are involved in transitional microvascular tone dysregulation in the pr... [more]

© 2015 Dyson et al.Background & Aims: Hydrogen sulphide (H2S), nitric oxide (NO), and carbon monoxide (CO) are involved in transitional microvascular tone dysregulation in the preterm infant; however there is conflicting evidence on the interaction of these gasotransmitters, and their overall contribution to the microcirculation in newborns is not known. The aim of this study was to measure the levels of all 3 gasotransmitters, characterise their interrelationships and elucidate their combined effects on microvascular blood flow. Methods: 90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as nitrate and nitrite in urine. H2S was measured as thiosulphate by liquid chromatography. Relationships between levels of the gasotransmitters and microvascular blood flow were assessed through partial correlation controlling for the influence of gestational age. Structural equation modelling was used to examine the combination of these effects on microvascular blood flow and derive a theoretical model of their interactions. Results: No relationship was observed between NO and CO (p = 0.18, r = 0.18). A positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = -0.33) exists. Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit is presented. Conclusions: The relationships between NO and H2S, and CO and H2S may be of importance in the preterm newborn, particularly as NO levels in males are associated with higher H2S levels and higher microvascular blood flow and CO in females appears to convey protection against vascular dysregulation. Here we present a theoretical model of these interactions and their overall effects on microvascular flow in the preterm newborn, upon which future mechanistic studies may be based.

DOI 10.1371/journal.pone.0121621
Citations Scopus - 2
Co-authors Ian Wright, Joanna Latter
2015 Palliser HK, Kelleher MA, Tolcos M, Walker DW, Hirst JJ, 'Effect of postnatal progesterone therapy following preterm birth on neurosteroid concentrations and cerebellar myelination in guinea pigs', Journal of Developmental Origins of Health and Disease, 6 350-361 (2015) [C1]

© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2015.Allopregnanolone protects the fetal brain and promotes normal deve... [more]

© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2015.Allopregnanolone protects the fetal brain and promotes normal development including myelination. Preterm birth results in the early separation of the infant from the placenta and consequently a decline in blood and brain allopregnanolone concentrations. Progesterone therapy may increase allopregnanolone and lead to improved oligodendrocyte maturation. The objectives of this study were to examine the efficacy of progesterone replacement in augmenting allopregnanolone concentrations during the postnatal period and to assess the effect on cerebellar myelination - a region with significant postnatal development. Preterm guinea pig neonates delivered at 62 days of gestation by caesarean section received daily s.c. injections of vehicle (2-Hydroxypropyl-ß-cyclodextrin) or progesterone (16 mg/kg) for 8 days until term-equivalent age (TEA). Term delivered controls (PND1) received vehicle. Neonatal condition/wellbeing was scored, and salivary progesterone was sampled over the postnatal period. Brain and plasma allopregnanolone concentrations were measured by radioimmunoassay; cortisol and progesterone concentrations were determined by enzyme immunoassay; and myelin basic protein (MBP), proteolipid protein (PLP), oligodendroctye transcription factor 2 (OLIG2) and platelet-derived growth factor receptor-a (PDGFRa) were quantified by immunohistochemistry and western blot. Brain allopregnanolone concentrations were increased in progesterone-treated neonates. Plasma progesterone and cortisol concentrations were elevated in progesterone-treated male neonates. Progesterone treatment decreased MBP and PLP in lobule X of the cerebellum and total cerebellar OLIG2 and PDGFRa in males but not females at TEA compared with term animals. We conclude that progesterone treatment increases brain allopregnanolone concentrations, but also increases cortisol levels in males, which may disrupt developmental processes. Consideration should be given to the use of non-metabolizable neurosteroid agonists.

DOI 10.1017/S2040174415001075
Citations Scopus - 2
Co-authors Jon Hirst
2014 Dyson RM, Palliser HK, Latter JL, Chwatko G, Glowacki R, Wright IMR, 'A Role for H2S in the microcirculation of newborns: The major metabolite of H2S (thiosulphate) is increased in preterm infants', PLoS ONE, 9 (2014) [C1]

Excessive vasodilatation during the perinatal period is associated with cardiorespiratory instability in preterm neonates. Little evidence of the mechanisms controlling microvascu... [more]

Excessive vasodilatation during the perinatal period is associated with cardiorespiratory instability in preterm neonates. Little evidence of the mechanisms controlling microvascular tone during circulatory transition exists. We hypothesised that hydrogen sulphide (H2S), an important regulator of microvascular reactivity and central cardiac function in adults and animal models, may contribute to the vasodilatation observed in preterm newborns. Term and preterm neonates (24-43 weeks gestational age) were studied. Peripheral microvascular blood flow was assessed by laser Doppler. Thiosulphate, a urinary metabolite of H2S, was determined by high performance liquid chromatography as a measure of 24 hr total body H2S turnover for the first 3 days of postnatal life. H2S turnover was greatest in very preterm infants and decreased with increasing gestational age (p = 0.0001). H2S turnover was stable across the first 72 hrs of life in older neonates. In very preterm neonates, H2S turnover increased significantly from day 1 to 3 (p = 0.0001); and males had higher H2S turnover than females (p = 0.04). A significant relationship between microvascular blood flow and H2S turnover was observed on day 2 of postnatal life (p = 0.0004). H2S may play a role in maintaining microvascular tone in the perinatal period. Neonates at the greatest risk of microvascular dysfunction characterised by inappropriate peripheral vasodilatation - very preterm male neonates - are also the neonates with highest levels of total body H2S turnover suggesting that overproduction of this gasotransmitter may contribute to microvascular dysfunction in preterms. Potentially, H2S is a target to selectively control microvascular tone in the circulation of newborns. © 2014 Dyson et al.

DOI 10.1371/journal.pone.0105085
Citations Scopus - 2Web of Science - 1
Co-authors Ian Wright, Joanna Latter
2014 Dyson RM, Palliser HK, Lakkundi A, de Waal K, Latter JL, Clifton VL, Wright IM, 'Early microvascular changes in the preterm neonate: a comparative study of the human and guinea pig.', Physiol Rep, 2 (2014) [C1]
DOI 10.14814/phy2.12145
Co-authors Joanna Latter, Ian Wright, Vicki Clifton
2014 Shaw JC, Palliser HK, Walker DW, Hirst JJ, 'Preterm birth affects GABAA receptor subunit mRNA levels during the foetal-to-neonatal transition in guinea pigs', Journal of Developmental Origins of Health and Disease, 6 250-260 (2014) [C1]

© 2015 Cambridge University Press and the International Society for Developmental Origins of Health and Disease.Modulation of gamma-aminobutyric acid A (GABAA) receptor signallin... [more]

© 2015 Cambridge University Press and the International Society for Developmental Origins of Health and Disease.Modulation of gamma-aminobutyric acid A (GABAA) receptor signalling by the neurosteroid allopregnanolone has a major role in late gestation neurodevelopment. The objective of this study was to characterize the mRNA levels of GABAA receptor subunits (a4, a5, a6 and d) that are key to neurosteroid binding in the brain, following preterm birth. Myelination, measured by the myelin basic protein immunostaining, was used to assess maturity of the preterm brains. Foetal guinea pig brains were obtained at 62 days' gestational age (GA, preterm) or at term (69 days). Neonates were delivered by caesarean section, at 62 days GA and term, and maintained until tissue collection at 24 h of age. Subunit mRNA levels were quantified by RT-PCR in the hippocampus and cerebellum of foetal and neonatal brains. Levels of the a6 and d subunits were markedly lower in the cerebellum of preterm guinea pigs compared with term animals. Importantly, there was an increase in mRNA levels of these subunits during the foetal-to-neonatal transition at term, which was not seen following preterm birth. Myelination was lower in preterm neonatal brains, consistent with marked immaturity. Salivary cortisol concentrations, measured by EIA, were also higher for the preterm neonates, suggesting greater stress. We conclude that there is an adaptive increase in the levels of mRNA of the key GABAA receptor subunits involved in neurosteroid action after term birth, which may compensate for declining allopregnanolone levels. The lower levels of these subunits in preterm neonates may heighten the adverse effect of the premature decline in neurosteroid exposure.

DOI 10.1017/S2040174415000069
Citations Scopus - 2
Co-authors Jon Hirst
2014 Hirst JJ, Kelleher MA, Walker DW, Palliser HK, 'Neuroactive steroids in pregnancy: Key regulatory and protective roles in the foetal brain', Journal of Steroid Biochemistry and Molecular Biology, 139 144-153 (2014) [C1]

Neuroactive steroid concentrations are remarkably high in the foetal brain during late gestation. These concentrations are maintained by placental progesterone synthesis and the i... [more]

Neuroactive steroid concentrations are remarkably high in the foetal brain during late gestation. These concentrations are maintained by placental progesterone synthesis and the interaction of enzymes in the placenta and foetal brain. 5a-Pregnane-3a-ol-20-one (allopregnanolone) is a key neuroactive steroid during foetal life, although other 3a-hydroxy- pregnanes may make an additional contribution to neuroactive steroid action. Allopregnanolone modulates GABAergic inhibition to maintain a suppressive action on the foetal brain during late gestation. This action suppresses foetal behaviour and maintains the appropriate balance of foetal sleep-like behaviours, which in turn are important to normal neurodevelopment. Neuroactive steroid-induced suppression of excitability has a key role in protecting the foetal brain from acute hypoxia/ischaemia insults. Hypoxia-induced brain injury is markedly increased if neuroactive steroid levels are suppressed and there is increased seizure activity. There is also a rapid increase in allopregnanolone synthesis and hence levels in response to acute stress that acts as an endogenous protective mechanism. Allopregnanolone has a trophic role in regulating development, maintaining normal levels of apoptosis and increasing myelination during late gestation in the brain. In contrast, chronic foetal stressors, including intrauterine growth restriction, do not increase neuroactive steroid levels in the brain and exposure to repeated synthetic corticosteroids reduce neuroactive steroid levels. The reduced availability of neuroactive steroids may contribute to the adverse effects of chronic stressors on the foetal and newborn brain. Preterm birth also deprives the foetus of neuroactive steroid mediated protection and may increase vulnerability to brain injury and suboptimal development. These finding suggest replacement therapies should be explored. This article is part of a Special Issue entitled 'Pregnancy and steroids © 2013 Elsevier Ltd. All rights reserved.

DOI 10.1016/j.jsbmb.2013.04.002
Citations Scopus - 10Web of Science - 5
Co-authors Jon Hirst
2014 Welsh TN, Hirst JJ, Palliser H, Zakar T, 'Progesterone Receptor Expression Declines in the Guinea Pig Uterus during Functional Progesterone Withdrawal and in Response to Prostaglandins', PLOS ONE, 9 (2014) [C1]
DOI 10.1371/journal.pone.0105253
Co-authors Jon Hirst
2014 Palliser HK, Kelleher MA, Welsh TN, Zakar T, Hirst JJ, 'Mechanisms Leading to Increased Risk of Preterm Birth in Growth-Restricted Guinea Pig Pregnancies', REPRODUCTIVE SCIENCES, 21 269-276 (2014) [C1]
DOI 10.1177/1933719113497268
Citations Scopus - 3
Co-authors Jon Hirst
2014 Cumberland AL, Palliser HK, Hirst JJ, 'Increased placental neurosteroidogenic gene expression precedes poor outcome in the preterm guinea pig', Journal of Developmental Origins of Health and Disease, 5 74-78 (2014) [C1]

Placental 5a-reductase (5aR) is influenced by in utero compromises and has a role in regulating neuroactive steroid concentrations in the fetus. The objective of this study was to... [more]

Placental 5a-reductase (5aR) is influenced by in utero compromises and has a role in regulating neuroactive steroid concentrations in the fetus. The objective of this study was to determine if changes in placental 5aR were associated with neonatal outcome after birth. Guinea pigs were delivered by cesarean section at term (GA69, n=22) or preterm (GA62, n=36) and the placenta collected. Preterm neonates were maintained for 24 h unless their condition deteriorated before this time. Enzyme mRNA expression of 5aR type-1 and 5aR type-2 were determined using real-time PCR. All preterm neonates had significantly higher 5aR2 expression in their placenta compared with placentae from term neonates (P<0.0001). Expression was also markedly higher in the placentae from neonates that did not survive until 24 h, compared with surviving preterm neonates (P=0.04). These findings suggest differences of in utero neurosteroidogenic capacity between surviving and non-surviving preterm guinea pig neonates. The increased 5aR2 mRNA expression in the placenta of non-survivors suggests an induction of the neurosteroid pathway due to prior exposure to an in utero compromise, with such exposure possibly a predisposing factor that contributed to their poor ex utero outcome. © 2014 Cambridge University Press.

DOI 10.1017/S2040174413000573
Co-authors Jon Hirst
2013 Bennett GA, Palliser HK, Saxby B, Walker DW, Hirst JJ, 'Effects of Prenatal Stress on Fetal Neurodevelopment and Responses to Maternal Neurosteroid Treatment in Guinea Pigs', DEVELOPMENTAL NEUROSCIENCE, 35 416-426 (2013) [C1]
DOI 10.1159/000354176
Citations Scopus - 8Web of Science - 5
Co-authors Jon Hirst
2013 Kelleher MA, Hirst JJ, Palliser HK, 'Changes in neuroactive steroid concentrations after preterm delivery in the guinea pig', Reproductive Sciences, 20 1365-1375 (2013) [C1]

Background: Preterm birth is a major cause of neurodevelopmental disorders. Allopregnanolone, a key metabolite of progesterone, has neuroprotective and developmental effects in th... [more]

Background: Preterm birth is a major cause of neurodevelopmental disorders. Allopregnanolone, a key metabolite of progesterone, has neuroprotective and developmental effects in the brain. The objectives of this study were to measure the neuroactive steroid concentrations following preterm delivery in a neonatal guinea pig model and assess the potential for postnatal progesterone replacement therapy to affect neuroactive steroid brain and plasma concentrations in preterm neonates. Methods: Preterm (62-63 days) and term (69 days) guinea pig pups were delivered by cesarean section and tissue was collected at 24 hours. Plasma progesterone, cortisol, allopregnanolone, and brain allopregnanolone concentrations were measured by immunoassay. Brain 5a-reductase (5aR) expression was determined by Western blot. Neurodevelopmental maturity of preterm neonates was assessed by immunohistochemistry staining for myelination, glial cells, and neurons. Results: Brain allopregnanolone concentrations were significantly reduced after birth in both preterm and term neonates. Postnatal progesterone treatment in preterm neonates increased brain and plasma allopregnanolone concentrations. Preterm neonates had reduced myelination, low birth weight, and high mortality compared to term neonates. Brain 5aR expression was also significantly reduced in neonates compared to fetal expression. Conclusions: Delivery results in a loss of neuroactive steroid concentrations resulting in a premature reduction in brain allopregnanolone in preterm neonates. Postnatal progesterone therapy reestablished neuroactive steroid levels in preterm brains, a finding that has implications for postnatal growth following preterm birth that occurs at a time of neurodevelopmental immaturity. © 2013 The Author(s).

DOI 10.1177/1933719113485295
Citations Scopus - 8Web of Science - 3
Co-authors Jon Hirst
2012 Palliser HK, Yates DM, Hirst JJ, 'Progesterone receptor isoform expression in response to in utero growth restriction in the fetal guinea pig brain', Neuroendocrinology, 96 60-67 (2012) [C1]
Citations Scopus - 5Web of Science - 4
Co-authors Jon Hirst
2012 Dyson RM, Palliser HK, Kelleher MA, Hirst JJ, Wright IM, 'The guinea pig as an animal model for studying perinatal changes in microvascular function', Pediatric Research, 71 20-24 (2012) [C1]
DOI 10.1038/pr.2011.9
Citations Scopus - 8Web of Science - 5
Co-authors Ian Wright, Jon Hirst
2012 Welsh T, Paul J, Palliser H, Hirst J, Mesiano S, Zakar T, 'PGDH Expression Decreases at Term before Labor Onset in Guinea Pig Fetal Membranes', REPRODUCTIVE SCIENCES, 19 192A-192A (2012) [C3]
Citations Web of Science - 1
Co-authors Jon Hirst, Jonathan Paul
2012 Welsh TN, Paul JW, Palliser HK, Tabatabaeehatambakhsh SH, Hirst JJ, Mesiano S, Zakar T, '15-hydroxyprostaglandin dehydrogenase expression and localization in guinea pig gestational tissues during late pregnancy and parturition', Reproductive Sciences, 19 1099-1109 (2012) [C1]
DOI 10.1177/1933719112442247
Citations Scopus - 2Web of Science - 2
Co-authors Jon Hirst, Jonathan Paul
2011 Kelleher MA, Palliser HK, Walker DW, Hirst JJ, 'Sex-dependent effect of a low neurosteroid environment and intrauterine growth restriction on foetal guinea pig brain development', Journal of Endocrinology, 208 301-309 (2011) [C1]
DOI 10.1677/joe-10-0248
Citations Scopus - 19Web of Science - 11
Co-authors Jon Hirst
2010 Palliser HK, Zakar T, Symonds IM, Hirst JJ, 'Progesterone receptor isoform expression in the guinea pig myometrium from normal and growth restricted pregnancies', Reproductive Sciences, 17 776-782 (2010) [C1]
DOI 10.1177/1933719110371517
Citations Scopus - 12Web of Science - 8
Co-authors Jon Hirst, Ian Symonds
2010 Dellios NL, Lappas M, Young IR, Palliser HK, Hirst JJ, Oliva K, et al., 'Increased expression of alpha-enolase in cervico-vaginal fluid during labour', European Journal of Obstetrics Gynecology and Reproductive Biology, 153 16-22 (2010) [C1]
DOI 10.1016/j.ejogrb.2010.06.014
Citations Scopus - 2Web of Science - 2
Co-authors Jon Hirst
2010 McKendry AA, Palliser HK, Yates DM, Walker DW, Hirst JJ, 'The effect of betamethasone treatment on neuroactive steroid synthesis in a foetal guinea pig model of growth restriction', Journal of Neuroendocrinology, 22 166-174 (2010) [C1]
DOI 10.1111/j.1365-2826.2009.01949.x
Citations Scopus - 22Web of Science - 15
Co-authors Jon Hirst
2009 Hirst JJ, Walker DW, Yawno T, Palliser HK, 'Stress in pregnancy: A role for neuroactive steroids in protecting the fetal and neonatal brain', Developmental Neuroscience, 31 363-377 (2009) [C1]
DOI 10.1159/000232555
Citations Scopus - 22Web of Science - 16
Co-authors Jon Hirst
2009 Vu TT, Hirst JJ, Stark MJ, Wright IM, Palliser HK, Hodyl NA, Clifton VL, 'Changes in human placental 5 alpha-reductase isoenzyme expression with advancing gestation: Effects of fetal sex and glucocorticoid exposure', Reproduction Fertility and Development, 21 599-607 (2009) [C1]
DOI 10.1071/rd08224
Citations Scopus - 16Web of Science - 15
Co-authors Ian Wright, Vicki Clifton, Jon Hirst
2008 Hirst JJ, Palliser HK, Roach DM, Yawno T, Walker DW, 'Neurosteroids in the fetus and neonate: Potential protective role in compromised pregnancies', Neurochemistry International, 52 602-610 (2008) [C1]
DOI 10.1016/j.neuint.2007.07.018
Citations Scopus - 23Web of Science - 17
Co-authors Jon Hirst
2007 Young R, Rice GE, Palliser HK, Ayhan M, Dellios NL, Hirst JJ, 'Identification of bactenecin-1 in cervicovaginal fluid by two-dimensional electrophoresis in an ovine model of preterm labour', Proteomics, 7 281-288 (2007) [C1]
DOI 10.1002/pmic.200500705
Citations Scopus - 5Web of Science - 6
Co-authors Jon Hirst
2007 Smith R, Van Helden DF, Hirst JJ, Zakar T, Read MA, Chan EC, et al., 'Pathological interactions with the timing of birth and uterine activation', Australian & New Zealand Journal of Obstetrics & Gynaecology, 47 430-437 (2007) [C1]
DOI 10.1111/j.1479-828x.2007.00775.x
Citations Scopus - 10Web of Science - 8
Co-authors Roger Smith, Jon Hirst, Dirk Vanhelden
2006 Palliser HK, Dellios N, Escalona R, Ooi G, Rice GE, Hirst J, Young IR, 'Labor-Associated Regulation of Prostaglandin E and F Synthesis and Action in the Ovine Amnion and Cervix', Reproductive Sciences, 13 19-24 (2006) [C1]
DOI 10.1016/j.jsgi.2005.09.009
Citations Scopus - 5Web of Science - 5
Co-authors Jon Hirst
2005 Hirst JJ, Parkington HC, Young IR, Palliser HK, Peri KG, Olsen DM, 'Delay of preterm birth in sheep by THG113.31, a prostaglandin F2[a] receptor antagonist', American Journal of Obstetrics and Gynecology, 193 256-266 (2005) [C1]
DOI 10.1016/j.ajog.2004.11.009
Citations Scopus - 23Web of Science - 22
Co-authors Jon Hirst
2005 Palliser HK, Hirst J, Ooi GT, Rice GE, Escalona RM, Dellios NL, et al., 'Prostaglandin E and F receptor expression and myometrial sensitivity at labour onset in sheep', Biology of Reproduction, 72 937-943 (2005) [C1]
DOI 10.1095/biolreprod.104.035311
Citations Scopus - 15Web of Science - 15
Co-authors Jon Hirst
2004 Palliser HK, Dellios N, Escalona R, Ooi G, Rice GE, Hirst J, Young IR, 'Changes in the Expression of prostaglandin E and F synthases at induced and spontaneous labour onset in the sheep', Journal of Endocrinology, 180 469-477 (2004) [C1]
DOI 10.1677/joe.0.1800469
Citations Scopus - 20Web of Science - 17
Co-authors Jon Hirst
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Conference (43 outputs)

Year Citation Altmetrics Link
2015 Saif Z, Dyson R, Palliser H, Wright I, Lu N, Clifton V, 'IDENTIFICATION OF SEVEN DIFFERENT ISOFORMS OF THE GLUCOCORTICOID RECEPTOR IN GUINEA PIG PLACENTA: RELATIONSHIP TO PRETERM DELIVERY, SEX AND BETAMETHASONE EXPOSURE', PLACENTA (2015) [E3]
Co-authors Ian Wright
2012 Bennett GA, Palliser HK, Kelleher MA, Saxby BM, Walker DW, Hirst JJ, 'Prenatal maternal psychosomatic stress: Effects on fetal brain development following maternal neurosteroid treatment in guinea pigs', Proceedings of the 39th Annual Meeting of the Fetal and Neonatal Physiological Society (2012) [E3]
Co-authors Jon Hirst
2012 Dyson RM, Palliser HK, Latter JL, Chwatko G, Glowacki R, Wright IM, 'Hydrogen sulphide in the neonatal transitional circulation', Proceedings of the 39th Annual Meeting of the Fetal and Neonatal Physiological Society (2012) [E3]
Co-authors Ian Wright, Joanna Latter
2012 Shepherd K, Palliser HK, Dyson RM, Wright IM, 'Regulation of microvascular blood fow by heme oxygenase in the preterm neonate', Proceedings of the 39th Annual Meeting of the Fetal and Neonatal Physiological Society (2012) [E3]
Co-authors Ian Wright
2012 Palliser HK, Kelleher MA, Saxby B, Walker DW, Hirst JJ, Bennett GA, 'Prenatal stress and effect of maternal neurosteroid treatment on fetal brain development in guinea pigs', Journal of Paediatrics and Child Health (2012) [E3]
Co-authors Jon Hirst
2012 Palliser HK, Hirst JJ, 'Vulnerability of compromised pregnancies to preterm labour', Journal of Paediatrics and Child Health (2012) [E3]
Co-authors Jon Hirst
2012 Welsh TN, Paul JW, Palliser HK, Hirst JJ, Mesiano S, Zakar T, 'PGDH expression decreases at term before labor onset in guinea pig fetal membranes', Reproductive Sciences (2012) [E3]
Co-authors Jon Hirst, Jonathan Paul
2011 Palliser HK, Welsh TN, Zakar T, Symonds IM, Hirst JJ, 'Changes to the balance of prostaglandin synthesis and metabolism with intrauterine growth restriction contributes to preterm labour in the guinea pig', Reproductive Sciences (2011) [E3]
Co-authors Jon Hirst, Ian Symonds
2011 Kelleher MA, Hirst JJ, Palliser HK, 'A guinea pig model for the study of neuroactive steroid replacement in the preterm neonatal brain', Reproductive Sciences (2011) [E3]
Co-authors Jon Hirst
2011 Dyson RM, Palliser HK, Wright IM, 'BAD EGGS AND BABIES; IS H2S A KEY PLAYER IN THE NEWBORN CIRCULATION?', PEDIATRIC RESEARCH (2011) [E3]
DOI 10.1038/pr.2011.515
2011 Dyson RM, Palliser HK, Wright IM, 'H2S; A novel player in the transitional microcirculation of preterm neonates?', Proceedings of The 38th Meeting of The Fetal and Neonatal Physiological Society (2011) [E3]
Co-authors Ian Wright
2011 Palliser HK, Welsh TN, Zakar T, Symonds IM, Hirst JJ, 'Intrauterine growth restriction leads to increased prostaglandin synthesis and reduced metabolism contributing to preterm labour in the guinea pig', Journal of Paediatrics and Child Health (2011) [E3]
Co-authors Ian Symonds, Jon Hirst
2011 Dyson RM, Palliser HK, Wright IM, 'Dysregulated microvascular flow in early extrauterine life in the pretern guinea pig', Journal of Paediatrics and Child Health (2011) [E3]
Co-authors Ian Wright
2011 Dyson RM, Palliser HK, Wright IM, 'Early microvascular blood flow changes: Evidence from human and guinea pig neonates', XIX NSW Scientific Meeting. Programme (2011) [E3]
Co-authors Ian Wright
2010 Dyson RM, Kelleher MA, Palliser HK, Hirst JJ, Wright IM, 'The guinea pig as an animal model for studying microvascular function in the preterm neonate in early extrauterine life', 9th World Congress for Microcirculation. Final Program and Abstract Book (2010) [E3]
Co-authors Ian Wright, Jon Hirst
2010 Dyson RM, Palliser HK, Kelleher MA, Hirst JJ, Wright IM, 'Preterm birth and intrauterine growth restriction: effect of microvascular function in the neonatal guinea pig', The Endocrine Society of Australia Annual Scientific Meeting Proceedings and Abstract Book (2010) [E3]
Co-authors Jon Hirst, Ian Wright
2010 Kelleher MA, Palliser HK, Hirst JJ, 'Premature birth results in ex utero brain development in a low neuroprotective steroid environment', The Endocrine Society of Australia Annual Scientific Meeting Proceedings and Abstract Book (2010) [E3]
Co-authors Jon Hirst
2010 Kelleher MA, Palliser HK, Hirst JJ, 'Compromised neurosteroid biosynthesis in the preterm neonate', Journal of Paediatrics and Child Health: Abstracts of the 14th Annual Congress of the Perinatal Society of Australia and New Zealand 2010 (2010) [E3]
Co-authors Jon Hirst
2010 Dyson RM, Kelleher MA, Palliser HK, Wright IM, 'The guinea pig as an animal model for perinatal vascular changes?', Journal of Paediatrics and Child Health: Abstracts of the 14th Annual Congress of the Perinatal Society of Australia and New Zealand 2010 (2010) [E3]
Co-authors Ian Wright
2009 McKendry AA, Palliser HK, Walker DW, Hirst JJ, 'The effect of betamethasone treatment on peripheral eurosteroidogenesis in a guinea pig model of growth restriction', Reproductive Sciences (2009) [E3]
Co-authors Jon Hirst
2009 Gibson KJ, Wang Y, Boyce AC, Palliser HK, Hirst JJ, Lumbers ER, 'Effects of intrauterine growth restriction on the intrarenal renin angiotensin system in the neonatal guinea pig', Journal of Paediatrics and Child Health (2009) [E3]
DOI 10.1111/j.1440-1754.2009.01474.x
Co-authors Jon Hirst
2009 Kelleher MA, Palliser HK, Walker DW, Hirst JJ, 'Effect of intrauterine growth restriction and pharmacologic inhibition of 5alpha-reductase on enzyme expression in the fetal cerebellum', Journal of Paediatrics and Child Health (2009) [E3]
DOI 10.1111/j.1440-1754.2009.01475.x
Co-authors Jon Hirst
2009 McKendry AA, Palliser HK, Walker DW, Hirst JJ, 'Effect of betamethasone treatment on steroidogenic enzyme expression in growth restricted fetal guinea pigs', Journal of Paediatrics and Child Health (2009) [E3]
DOI 10.1111/j.1440-1754.2009.01475.x
Co-authors Jon Hirst
2009 Palliser HK, Zakar T, Hirst JJ, 'Effect of growth restriction on myometrial progesterone receptor expression near term', Journal of Paediatrics and Child Health (2009) [E3]
DOI 10.1111/j.1440-1754.2009.01474.x
Co-authors Jon Hirst
2009 Roach DM, Hirst JJ, Palliser HK, 'Effect of IUGR and sex on PR expression in the fetal guinea pig brain', Journal of Paediatrics and Child Health (2009) [E3]
DOI 10.1111/j.1440-1754.2009.01475.x
Co-authors Jon Hirst
2008 Kelleher MA, Palliser HK, Roach DM, Sullivan RK, Walker DW, Hirst JJ, 'Effect of 5 alpha-reductase inhibition on apoptotic brain cell death and the expression of neurosteroidogenic enzymes in the fetal and neonatal guinea pig', Journal of Paediatrics and Child Health (2008) [E3]
DOI 10.1111/j.1440-1754.200801297.x
Co-authors Jon Hirst
2008 McKendry AA, Palliser HK, Roach DM, Sullivan RK, Walker DW, Hirst JJ, 'Repeated exposure to betamethasone increases brain cell death and suppresses neurosteroidogenic pathways in the growth restricted guinea pig fetus', Journal of Paediatrics and Child Health (2008) [E3]
DOI 10.1111/j.1440-1754.200801297.x
Co-authors Jon Hirst
2008 McKendry AA, Palliser HK, Roach DM, Sullivan RK, Walker DW, Hirst JJ, 'Effect of betamethasone treatment on brain cell death and neurosteroidogenic pathways in a guinea pig model of growth restriction', Reproductive Sciences (2008) [E3]
Co-authors Jon Hirst
2008 Kelleher MA, Palliser HK, Roach DM, Sullivan RK, Walker DW, Hirst JJ, 'Effect of inhibition of 5 alpha reduced steroid synthesis on apoptotic brain cell death and neurosteroidogenic enzyme expression in the fetal and neonatal guinea pig', Reproductive Sciences (2008) [E3]
Co-authors Jon Hirst
2008 Sullivan RK, Palliser HK, McKendry AA, Roach DM, Walker DW, Hirst JJ, 'Effect of betemethasone treatment on apoptotic cell death and neurosteriodogenic pathways in a guinea pig model of growth restriction', 2008 Neuroscience Meeting Planner (2008) [E3]
Co-authors Jon Hirst
2008 Smith AT, Palliser HK, Zakar T, Dunstan RH, Hirst JJ, 'Neurosteroid profiles in fetal, maternal and neonatal guinea pigs using gas chromatography-mass spectrometry', The Twenty-Second Fetal and Neonatal Workshop of Australia and New Zealand Abstract Book (2008) [E3]
Co-authors Jon Hirst, Hugh Dunstan
2007 Smith AT, Palliser HK, Hirst JJ, 'Measurement of neurosteroids in the fetal and neonatal guinea pig brain using gas chromatography-mass spectrometry', Fetal & Neonatal Workshop of Australia and New Zealand 21st Annual Meeting. Abstracts (2007) [E3]
Co-authors Jon Hirst
2007 Palliser HK, Roach DM, Walker DW, Hirst JJ, 'Expression of 5aReductase enzymes in the fetal guinea pig brain and placenta following intrauterine growth restriction', Reproductive Sciences (Scientific Program & Abstracts: 54th Annual Meeting, SGI) (2007) [E3]
Co-authors Jon Hirst
2007 Roach DM, Palliser HK, Walker DW, Hirst JJ, 'Expression of 5aReductase enzymes in uterine tissues at term and following labor', Reproductive Sciences (Scientific Program & Abstracts: 54th Annual Meeting, SGI) (2007) [E3]
Co-authors Jon Hirst
2007 Palliser HK, Roach DM, Walker DW, Hirst JJ, 'Effect of intrauterine growth restriction on the expression of 5alpha reductase in the fetal guinea pig brain and placenta', Satellite Conference of DOHaD 2007 (5th World Congress of Developmental Origins of Health and Disease) (2007) [E3]
Co-authors Jon Hirst
2005 Palliser HK, Hirst JJ, Rice GE, Dellios NL, Escalona RM, Ooi GT, Young IR, 'The NF kappa B inhibitor, sulfasalazine, suppresses uterine activity by a PGHS- independent pathway.', JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION (2005)
Co-authors Jon Hirst
2004 Palliser HK, Dellios N, Escalona R, Rice GE, Hirst JJ, Young IR, '2004 Changes in prostaglandin receptor expression in the amnion and cervix following preterm and term labour', Endocrine Society of Australian 47th Annual Meeting (2004) [E3]
Co-authors Jon Hirst
2004 Palliser HK, Hirst JJ, Rice GE, Dellios NL, Escalona RM, Ooi GT, Young IR, 'Expression of prostaglandin E and F receptors in ovine gestational tissues at labour onset', Perinatal Society of Australia and New Zealand 7th Annual Meeting (2004) [E3]
Co-authors Jon Hirst
2004 Palliser HK, Hirst JJ, Rice GE, Dellios NL, Escalona RM, Ooi GT, Young IR, 'Increase in the expression of prostaglandin F synthase in ovine gestational tissues at labor onset.', JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION (2004)
Co-authors Jon Hirst
2004 Hirst JJ, Young IR, Palliser HK, Peri KG, Zaragoza DB, Olson DM, 'Delay of preterm birth in sheep by THG113.31, a prostaglandin (PG)F-2 alpha receptor (FP) antagonist: Electromyographic activity (EMG), blood gases, and PGs.', JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION (2004)
Co-authors Jon Hirst
2004 Parkington HC, Hirst JJ, Young IR, Palliser HK, Palliser DM, 'THG-113, a prostaglandin F2a (PGF2a) receptor antagonist suppresses the sensitivity to maximal contractile activity evoked by exogenous PGF2a in isolated sheep myometrium', Society for Gynecologic Investigation 51st Annual Meeting (2004) [E3]
Co-authors Jon Hirst
2004 Palliser HK, Dellios N, Escalona R, Ooi G, Rice GE, Hirst JJ, '2004 Prostaglandin F and E synthases in ovine myometrium, endometrium and placenta during at labour onset', Society for Gynecologic Investigation 51st Annual Meeting (2004) [E3]
Co-authors Jon Hirst
2004 Hirst JJ, Young IR, Palliser HK, Peri KG, Zaragoza DB, Olson DM, '2004 delay of preterm birth in sheep by THG-113, a prostaglandin F2a receptor antagonist: electromyographic activity, blood gases and PGs', Society for Gynecologic investigation 51st annual meeting (2004) [E3]
Co-authors Jon Hirst
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Grants and Funding

Summary

Number of grants 14
Total funding $1,926,522

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


20161 grants / $21,745

Reduced neurosteroid stimulation following preterm birth adversely affects long-term patterns of behaviour $21,745

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Hannah Palliser, Professor Jon Hirst, Doctor Rebecca Glover
Scheme Research Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600447
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20151 grants / $1,151,520

Perinatal stress leads to neurosteroid deficits and adverse behavioural outcomes$1,151,520

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Jon Hirst, Associate Professor David Walker, Doctor Hannah Palliser, Professor Deborah Hodgson
Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1400014
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

20142 grants / $47,512

Progesterone therapy for preterm labour - evaluation of effects on fetal neuroactive steroid profiles$27,512

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Jon Hirst, Professor Ian Symonds, Doctor Hannah Palliser
Scheme Research Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1400122
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Stress in pregnancy and poor neurodevelopmental outcomes in children: the role of miRNA in regulating neurosteroid dysfunction$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Hannah Palliser, Professor Jon Hirst
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1401439
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20121 grants / $34,454

Disruption of gestational neurosteroid concentrations by stressful events leads to adverse neurodevelopmental and behavioural outcomes in children form these pregnancies$34,454

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Jon Hirst, Professor Ian Symonds, Doctor Hannah Palliser
Scheme Research Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1200176
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20111 grants / $2,000

Society for Gynecologic Investigation (SGI), Miami, Florida, USA, 16 - 19 March 2011$2,000

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Hannah Palliser
Scheme Travel Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100147
Type Of Funding Internal
Category INTE
UON Y

20101 grants / $23,025

Investigation of IUGR-associated preterm labour using a guinea pig model$23,025

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Hannah Palliser, Professor Jon Hirst, Professor Ian Symonds
Scheme Research Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo G1000119
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20091 grants / $13,470

i-STAT 1 Blood Gas Analyser and Softron BP-98E$13,470

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Conjoint Professor Ian Wright, Professor Jon Hirst, Professor Eugenie Lumbers, Conjoint Professor Tamas Zakar, Doctor Hannah Palliser
Scheme Equipment Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189843
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20082 grants / $24,808

Does fetal growth restriction increase uterine activity and upregulate labour associated genes preterm?$15,208

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Jon Hirst, Doctor Hannah Palliser, Professor Ian Symonds
Scheme Research Grant
Role Investigator
Funding Start 2008
Funding Finish 2008
GNo G0189368
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

LED fluorescence illuminators and filter set (525nm + 575DF20) for LAS3000 image analysis system$9,600

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Roger Smith, Professor Ian Symonds, Conjoint Associate Professor Andrew Bisits, Conjoint Professor Tamas Zakar, Doctor John Fitter, Doctor Cheng Chan, Conjoint Associate Professor Rick Nicholson, Doctor Giavanna Angeli, Doctor Kaushik Maiti, Doctor Jonathan Paul, Professor Jon Hirst, Doctor Hannah Palliser, Professor Eugenie Lumbers
Scheme Equipment Grant
Role Investigator
Funding Start 2008
Funding Finish 2008
GNo G0188543
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20074 grants / $607,988

2007 Research Fellowship - PRCRS$565,618

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Hannah Palliser
Scheme Research Fellowship
Role Lead
Funding Start 2007
Funding Finish 2012
GNo G0187107
Type Of Funding Internal
Category INTE
UON Y

Beta Radiation Counter Instrument facility$25,670

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Roger Smith, Conjoint Associate Professor Vicki Clifton, Conjoint Professor Tamas Zakar, Conjoint Associate Professor Rick Nicholson, Dr Mark Read, Doctor Cheng Chan, Doctor John Fitter, Conjoint Associate Professor Andrew Bisits, Professor Jon Hirst, Doctor Hannah Palliser, Professor Ian Symonds
Scheme Equipment Grant
Role Investigator
Funding Start 2007
Funding Finish 2007
GNo G0188194
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

2007 Research Fellowship Project Grant$15,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Hannah Palliser
Scheme Fellowship Grant
Role Lead
Funding Start 2007
Funding Finish 2007
GNo G0188119
Type Of Funding Internal
Category INTE
UON Y

Society of Gynecologic Investigation, 14-17 March 2007$1,700

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Hannah Palliser
Scheme Travel Grant
Role Lead
Funding Start 2007
Funding Finish 2007
GNo G0187373
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Number of supervisions

Completed4
Current3

Total current UON EFTSL

PhD1.4

Current Supervision

Commenced Level of Study Research Title / Program / Supervisor Type
2015 PhD Perinatal Stress and its Effect on Neurosteroid Levels and Behavioural Outcomes
PhD(Experimental Pharmacology), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2014 PhD Neurosteroidogenesis, Neurodevelopment and Behaviour Following Preterm Birth: Effect of Prenatal and Postnatal Therapies
PhD(Experimental Pharmacology), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2013 PhD Affect of Prenatal Insults on Long-Term Behaviour and Neurodevelopment; and Potential Neurosteroid Replacement Therapy
PhD(Experimental Pharmacology), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor

Past Supervision

Year Level of Study Research Title / Program / Supervisor Type
2015 PhD The Effects of Maternal Stress on Perinatal Neurodevelopment and Behaviour
PhD(Experimental Pharmacology), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2015 PhD Understanding Microvascular Function in Preterm Neonates
PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2012 PhD Potential Neurosteroid Replacement Therapy Following Premature Birth and Fetal Growth Restriction
PhD(Experimental Pharmacology), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2010 Masters Betamethasone: A Neuroactive Steroid Deficit and Adverse Effects in the Brain?
M Philosophy (Exper Pharmacol), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
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Dr Hannah Palliser

Position

Research Fellow
Mothers and Babies Research Centre
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Focus area

Pharmacy and Experimental Pharmacology

Contact Details

Email hannah.palliser@newcastle.edu.au
Phone (02) 4042 0371

Office

Building HMRI
Location Level 3 East

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