Mr Ryan Duchatel

Mr Ryan Duchatel

Research Assistant

School of Biomedical Sciences and Pharmacy (Medical Biochemistry)

Career Summary

Biography

Ryan is a passionate scientist with an interest in molecular mechanisms of cancer, in particular blood and brain cancers such as Acute Myeloid Leukaemia and paediatric glioma. Ryan currently works as a Research Assistant in the Molecular Oncology laboratory of Dr Matt Dun working on both in vitro and in vivo models of Leukaemia and Diffuse Intrinsic Pontine Glioma.

Ryan studied Biomedical Science graduating with First Class Honours in 2013 and is nearing completion of a PhD in Experimental Pharmacology from the University of Newcastle, Australia. Ryan has been the recipient of prestigious PhD Scholarships including the Ian Scott PhD Scholarship in Mental Health from Australian Rotary Health and the A.M Wood PhD Scholarship from the Schizophrenia Research Institute. 

Ryans PhD has focused on the neurobiology and genetics underpinning schizophrenia conducting studies examining how infections during pregnancy contribute to the development of schizophrenia in subsequent offspring. In particular, Ryan is investigating why people with schizophrenia have more inhibitory interneurons in the white matter underneath the cortex of brain and how maternal immune activation relates to this. Throughout his PhD, Ryan has developed extensive skills in cellular and molecular biology, including utilising both in vitro and in vivo models. 

Qualifications

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

Keywords

  • Neurobiology
  • Neuroscience
  • Schizophrenia
  • Cancer Biology
  • Brain Cancer
  • Molecular Oncology

Fields of Research

Code Description Percentage
110106 Medical Biochemistry: Proteins and Peptides (incl. Medical Proteomics) 20
111201 Cancer Cell Biology 80
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (3 outputs)

Year Citation Altmetrics Link
2018 Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Increased complement component 4 (C4) gene expression in the cingulate cortex of rats exposed to late gestation immune activation.', Schizophr Res, (2018)
DOI 10.1016/j.schres.2018.03.035
Co-authors Deborah Hodgson, Phillip Jobling, Douglas Smith, Pat Michie, Paul Tooney, Lauren Harms
2018 Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Late gestation immune activation increases IBA1-positive immunoreactivity levels in the corpus callosum of adult rat offspring', Psychiatry Research, 266 175-185 (2018)

© 2018 Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and c... [more]

© 2018 Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine upregulation may have key roles in schizophrenia neuropathology. We hypothesised that maternal immune activation induces changes in microglia and cytokines in the brains of the adult offspring. Maternal immune activation was induced by injecting polyriboinosinic:polyribocytidylic acid into pregnant rats on gestational day (GD) 10 or GD19, with brain tissue collected from the offspring at adulthood. We observed no change in Iba1, Gfap, IL1-ß and TNF-a mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP+IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP+IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring.

DOI 10.1016/j.psychres.2018.05.063
Co-authors Phillip Jobling, Douglas Smith, Rohan Walker, Paul Tooney, Deborah Hodgson, Lauren Harms, Pat Michie
2016 Duchatel RJ, Jobling P, Graham BA, Harms LR, Michie PT, Hodgson DM, Tooney PA, 'Increased white matter neuron density in a rat model of maternal immune activation - Implications for schizophrenia', Progress in Neuro-Psychopharmacology and Biological Psychiatry, 65 118-126 (2016) [C1]

© 2015. Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (I... [more]

© 2015. Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (IWMN) density in the fibre tracts below the cortex in people with schizophrenia. The current study assesses IWMN pathology in a model of maternal immune activation (MIA); a risk factor for schizophrenia. Experimental MIA was produced by an injection of polyinosinic:polycytidylic acid (PolyI:C) into pregnant rats on gestational day (GD) 10 or GD19. A separate control group received saline injections. The density of neuronal nuclear antigen (NeuN < sup > + < /sup > ) and somatostatin (SST < sup > + < /sup > ) IWMNs was determined in the white matter of the corpus callosum in two rostrocaudally adjacent areas in the 12week old offspring of GD10 (n=10) or GD19 polyI:C dams (n=18) compared to controls (n=20). NeuN < sup > + < /sup > IWMN density trended to be higher in offspring from dams exposed to polyI:C at GD19, but not GD10. A subpopulation of these NeuN < sup > + < /sup > IWMNs was shown to express SST. PolyI:C treatment of dams induced a significant increase in the density of SST < sup > + < /sup > IWMNs in the offspring when delivered at both gestational stages with more regionally widespread effects observed at GD19. A positive correlation was observed between NeuN < sup > + < /sup > and SST < sup > + < /sup > IWMN density in animals exposed to polyI:C at GD19, but not controls. This is the first study to show that MIA increases IWMN density in adult offspring in a similar manner to that seen in the brain in schizophrenia. This suggests the MIA model will be useful in future studies aimed at probing the relationship between IWMNs and schizophrenia.

DOI 10.1016/j.pnpbp.2015.09.006
Citations Scopus - 3Web of Science - 2
Co-authors Paul Tooney, Deborah Hodgson, Phillip Jobling, Pat Michie, Lauren Harms, Brett Graham

Conference (1 outputs)

Year Citation Altmetrics Link
2015 Duchatel R, Jobling P, Graham B, Harms L, Michie P, Hodgson D, Tooney P, 'Modelling white matter neuron pathology in schizophrenia using maternal immune activation', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Co-authors Paul Tooney, Deborah Hodgson, Phillip Jobling, Pat Michie, Lauren Harms, Brett Graham
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Mr Ryan Duchatel

Position

Research Assistant
Molecular Oncology
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Focus area

Medical Biochemistry

Contact Details

Email ryan.duchatel@newcastle.edu.au
Phone (02) 49854489
Mobile (+61) 419268714

Office

Room LS339
Building Life Science
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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