INABILITY TO REGULATE FATTY ACID OXIDATION OR GLYCOLYSIS INCREASES RENAL FIBROSIS

M LEE1,2, P MOUNT1, M KATERELOS1, K GLEICH1, D POWER1,2
1Austin Health, Heidelberg, Australia, 2Department of Medicine, The University of Melbourne, Heidelberg, Australia

Aim: To determine the roles of fatty acid oxidation (FAO) and glycolysis in renal fibrosis.
Background: Changes in energy metabolism are emerging as a key contributor in renal fibrosis. Expression of genes regulating fatty acid metabolism is reduced in fibrotic kidneys and aerobic glycolysis increases in renal disease models.
Methods: Mice with knock-in mutations of phosphosites in acetyl CoA carboxylase 1 and 2 (ACC1/2KI mice), the major regulator of FAO, and 6-phosphofructo-2kinase/fructose-2,6-biphosphatase (PFKFB2KI mice), the major regulator of glycolysis, were used to assess the roles of FAO and glycolysis, respectively. The folic acid nephropathy (FAN) and unilateral ureteric obstruction (UUO) models were induced in male ACC1/2KI and PFKFB2KI mice. Metformin was administered to mice with FAN.
Results: ACC Ser79 phosphorylation was reduced in folate-treated tubular epithelial cells (p<0.01) and WT mice with FAN (p<0.05). Mutation of these sites in ACC1/2 KI mice with FAN or UUO caused lipid accumulation (Oil Red O p<0.01), increased triglyceride (p<0.01), increased collagen (PicroSirius red p<0.001; Masson’s Trichrome p<0.01; qRT-PCR p<0.01) and increased α-SMA (Western blot p<0.05; qRT-PCR p<0.01). Metformin administration was associated with reduced fibrosis (PicroSirius red p<0.01) and lipid accumulation (Oil Red O p<0.05) in WT mice, but not in ACC1/2KI mice. To determine the role of glycolysis, UUO was induced in PFKFB2KI mice. WT mice with UUO had reduced PFKFB2 Ser483 phosphorylation (p<0.01). PFKFB2KI UUO mice had increased collagen (Picrosirius red p<0.001), increased fibronectin (Western blot p<0.05; qRT-PCR p<0.05) increased α-SMA (Western blot, p<0.05) and glycogen accumulation (PAS, p<0.05).
Conclusions: These data suggest reduced FAO and glycolysis is deleterious following renal injury. Phosphorylation of ACC reduces renal fibrosis and is essential for the anti-fibrotic effect of metformin.


Biography:
Mardiana Lee completed her advanced training in nephrology through  the Austin and the Royal Melbourne Hospital. She received her fellowship from the Royal Australasian College of Physician in 2015. She is currently completing her PhD at the University of Melbourne.

KCA3.1 MEDIATED DYSREGULATION OF MITOCHONDRIAL QUALITY CONTROL IN DIABETIC NEPHROPATHY

C HUANG1, H YI1, Y SHI1, Q CAO1, X-M CHEN1, C POLLOCK1
1University of Sydney, St Leonards, Australia

Aim: To identify the role of KCa3.1 in mitochondrial quality control in diabetic nephropathy.
Background: Mitochondrial dysfunction is involved in the pathogenesis of diabetic nephropathy. Mitochondrial quality control is characterized by repairing of mitochondrial damage through mitophagy and fission/fusion. It has been shown that blockade of KCa3.1, a potassium channel, ameliorates diabetic renal fibrosis and KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. However, the role of KCa3.1 in mitochondrial quality control is not yet known.
Methods: In vitro human proximal tubular cells (HK2 cells) transfected with scrambled siRNA or KCa3.1 siRNA were exposed to TGF-β1 for 48h. Mitochondrial function and mitochondrial ROS (mtROS) production were assessed. In vivo, diabetes was induced in KCa3.1+/+ and KCa3.1-/- mice by streptozotocin injection. The pro-fission protein dynamin-related protein 1 (Drp1) and pro-fussion protein mitofusin 2 (Mfn2) as well as BCL2 interacting protein 3 (BNIP3) (a mitophagy regulator) were examined by western blotting in HK2 cells and mice kidneys.
Results: The in vitro results showed that TGF-β1 significantly inhibited mitochondrial ATP production rate, compared to the controls, which were significantly reversed by KCa3.1 siRNA in HK2 cells. KCa3.1 gene silencing inhibited TGF-β1-induced significant increase in MitoSOX Red fluorescence in HK2 cells. TGF-β1 significantly increased the expression of Drp1 and BNIP3 in HK2 cells, which were attenuated by KCa3.1 gene silencing. The expression of Mfn2 was not overtly apparent on TGF-β1 stimulation. Consistently, the in vivo results showed significantly increased Drp1 and BNIP3 expression in diabetic KCa3.1 +/+ mice, which were significantly reduced in diabetic KCa3.1-/- mice.
Conclusions: KCa3.1 mediates dysregulation of mitochondrial quality control in diabetic nephropathy.


Biography:
Dr Chunling Huang is a NHMRC early career research fellow in the renal lab at Kolling Institute, University of Sydney. She has expertise in diabetic kidney disease, animal models of diabetic nephropathy and kidney fibrosis. Her research focuses on the novel therapeutic targets for chronic kidney diseases and the underling mechanisms including inflammation, fibrosis, fibroblast activation and autophagy.

 

NADPH-OXIDASE NOX5 AGGRAVATES RENAL INJURY IN THE AKITA MOUSE MODEL OF DIABETIC NEPHROPATHY

J JHA1, R TOUYZ2, C KENNEDY3, M COOPER1, K JANDELEIT-DAHM1
1Department Of Diabetes, Melbourne, Australia, 2Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom, 3Department of Medicine, Ottawa Hospital Research Institute, Ottawa, Canada

Background: Renal reactive oxygen species (ROS) play an important role in mediating kidney injury in diabetes. Increasing evidence suggests that the pro-oxidant enzyme, Nox5 plays a significant role in human diabetic nephropathy (DN). Nox5 is present in humans and rabbits but not in mice or rats. Thus, there is a paucity of information about Nox5 in conventional animal models of DN. We examined the role of Nox5 in the insulin deficient diabetic Akita mice model using human inducible transgenic mice that express Nox5 selectively in endothelial cells (VEcad+Nox5+) or in mesangial cells (SM22+Nox5+).
Methods: At week 10 mice were culled and kidneys were removed for the assessment of structural damage as well as gene and protein expression of markers of inflammation, fibrosis and oxidative stress. Protein expression of Nox5 and its localization in glomerular cells (endothelial and mesangial cells) were examined in transgenic mice by immunostaining.
Results: Expression of Nox5 was confirmed in glomerular endothelial and mesangial cells of transgenic mice. Diabetes induced increase in glomerulosclerosis, gene and protein expression of fibronectin and MCP-1 as well as nitrotyrosine were further increase in both diabetic Nox5 transgenic mice.
Conclusions: These findings suggest that Nox5 expression in endothelial or mesangial cells in an streptozotocin independent model of type 1 diabetes is associated with increased ROS production and accelerates renal injury in diabetes.


Biography:
Prof Jandeleit-Dahm is a physician scientist  and nephrologist. Her main research focus is the role of reactive oxygen species in the kidney and in cardiovascular complications of diabetes.

CYCLOPHILIN INHIBITION ATTENUATES RENAL FIBROSIS IN THE OBSTRUCTED KIDNEY

KG LEONG1,2, E OZOLS1,2, J KANELLIS1,2, J LILES3,D NIKOLIC-PATERSON1,2, F MA1,2
1Department of Nephrology, Monash Medical Centre, Clayton, Australia, 2Centre for Inflammatory Disease, Monash University, Clayton, Australia, 3Gilead Sciences, Foster City, USA

Aims: Determine whether therapeutic inhibition of cyclophilin (Cyp) function can suppress renal fibrosis in unilateral ureteric obstruction (UUO) and if cyclophilin A (CypA) has a specific role in this response.
Background: Cyclophilins are enzymes that regulate protein folding. Within this enzyme family, CypA promotes leukocyte recruitment and inflammation while CypD facilitates mitochondrial-dependent cell death. However, the role of cyclophilins in renal fibrosis is poorly understood.
Methods: C57BL/6J mice underwent UUO surgery and were killed on day 7; groups (n=10) were treated with 30mg/kg/BID of a pan-cyclophilin inhibitor (CYPi, which does not block calcineurin function) or vehicle by oral gavage from 1hr before surgery and continued to day 7. In addition, groups (n=10) of CypA-/- and wild type mice were killed on day 7 post-UUO. Controls had no UUO surgery.
Results: Compared to vehicle, CYPi treatment significantly reduced renal fibrosis in the obstructed kidney based on ↓37% collagen IV and ↓22% α-SMA staining area (P<0.01 vs vehicle) and reduced mRNA levels of α-SMA, collagen I, III and IV and TGF-b1 (all P<0.01 vs vehicle). CYPi treatment also reduced TUNEL+ apoptotic tubular cells by 60%, and reduced macrophage infiltration (P<0.001 vs vehicle). By contrast, CypA-/- mice showed no difference in renal fibrosis or in the infiltration of macrophages or T cells compared to wild type UUO mice.
Conclusions: Cyclophilins contribute to the development of renal fibrosis, inflammation and tubular apoptosis in obstructed kidney, although this does not involve CypA. Therapeutic targetting of cyclophilins, independent of calcineurin function, has potential for the treatment of renal fibrosis.


Biography:
Nephrologist undergoing my lab-based PhD studies at Department of Nephrology, Monash Health.

PRECLINICAL ASSESSMENT OF ANTI-MIDKINE ANTIBODIES IN REDUCING KIDNEY INJURY AND DYSFUNCTION INDUCED BY ADRIAMYCIN NEPHROPATHY

J WANG1, Q CAO1, Y WANG1, D HARRIS1, G ROBERTSON2, D BURG2, M HALASZ2, V LEE1
1Westmead Institute Of Medical Research, Westmead, Australia, 2Cellmid Limited, Sydney, Australia

Aim: To determine the efficacy of anti-Midkine (MK) antibodies in ameliorating kidney damage and dysfunction in the Adriamycin (ADR) nephropathy model.
Background: MK is known for its role in development and cancer where it promotes cell survival, proliferation and migration. Additionally, MK is implicated in inflammation and autoimmunity where it modulates chemotaxis, chemokine expression and immunological tolerance. Clinical studies have found progressive increases in systemic and urinary MK levels related to disease severity in chronic kidney disease (CKD)1-CKD5 patients. MK levels are also elevated in diverse experimental kidney disease models post injury or pathogenesis, and are associated with renal inflammation, fibrosis and progressive injury. More importantly, MK-deficient mice exhibit markedly reduced glomerulosclerosis, tubulointerstitial inflammation and damage than MK +/+ mice in ischaemic, diabetic and nephrectomy models, suggesting that MK’s pathological role in exacerbating renal injury and dysfunction operates primarily via its immunomodulatory functions.
Methods: ADR was administered once to male Balb/c mice via tail vein injections. Anti-MK antibodies were administered in prophylaxis mode by intraperitoneal injections to ADR-treated mice prior to ADR treatment, as well as periodically following treatment. All mice were sacrificed after 27 days for subsequent tissue processing and biochemical analysis for assessment of renal histology and function.
Results: ADR-treated mice administered with anti-MK antibodies exhibited significantly reduced overall kidney tissue damage in contrast with those administered with vehicle. Reduced proteinuria, serum creatinine and improved serum albumin levels were also observed in anti-MK antibody administered mice.
Conclusions: Our results indicate that MK plays a crucial role in modulating kidney injury and dysfunction in a murine model of FSGS, and therapeutic antibodies against MK may contribute to the treatment of chronic proteinuric renal disease.


Biography:
Jeffrey Wang is a second year PhD student under the renal department at the Westmead Institute of Medical Research. He is currently under the supervision of Assoc. Prof Vincent Lee from the Westmead Hospital, and Assoc. Prof Graham Robertson from Cellmid Limited. Jeffrey completed his bachelor degree with honours in science from the University of New South Wales in 2015, majoring in cellular biology and biochemistry. He began his PhD candidature at the Westmead Institute in 2016, and his current research focuses on exploring therapeutic options behind the molecule Midkine and inflammation and fibrosis in chronic kidney disease.

BLOCKADE OF RIPK3 MODIFIES RENAL FIBROGENESIS THROUGH INHIBITION OF NF ΚB

Y SHI1,  C HUANG1, X CHEN1, C POLLOCK1
1Kolling Institute, Royal North Shore Hospital, St Leonards, Australia

Aim: To define the role of receptor-interacting protein kinase 3 (RIPK3) in alleviating renal fibrogenesis.
Background: Current therapies for renal fibrosis are largely ineffective. Therefore, identification of novel therapeutic targets is essential. RIPK3 is identified as a crucial regulator of Interleukin-1 (IL-1) secretion via the necroptotic pathway and the nuclear factor NF κB pathway, which have been well recognised to be involved in renal fibrogenesis by regulating TGF-β. To date, the function of RIPK3 in renal fibrosis remains unclear.
Methods: C57BL/6 wild-type mice and C57BL/6 RIPK3 gene knock out (RIPK3-/-) mice were used in the study. Renal fibrosis was induced with folic acid (250 mg/kg) and animals were killed at 28th day after folic acid injection. Dabrafenib (2.5 μg/hr) was used as a pharmacological inhibitor of RIPK3.
Results: FA nephropathy led to a significant renal injury within in the kidney cortex characterized by tubular dilation, tubule atrophy, cast formation and inflammatory cell infiltration (p<0.0001). These pathological changes were accompanied by an elevation in expression of pro‐fibrotic markers (collagen I, p<0.05; collagen III, p<0.05; TGF-β, p<0.0001), myofibroblast activation (α-SMA, p<0.0001) and inflammatory response (MCP-1, p<0.0001; F4/80, p<0.0001, phosphorylated p65, p<0.01). Genetic ablation of RIPK3 or RIPK3 inhibition abrogated all markers of renal injury (all p<0.05), fibrotic responses (all p<0.05) and inflammation (all p<0.05). However, IL-1 production was not modified.
Conclusions: These results suggest that RIPK3 may be a potential novel target in renal fibrosis. However, the beneficial effects are likely to be mediated through inhibition of NFKB and independent of the necroptotic pathway.


Biography:
Ying Shi is is a PhD candidate in Medicine at the University of Sydney under the supervision of Prof. Carol Pollock. Her research focuses on identifying novel therapeutic target for renal fibrosis.

THE ROLE OF CILIAL PROTEIN#1 IN DIABETIC KIDNEY DISEASE (DKD)

S REDZEPAGIC1, C HUANG1, C POLLOCK1, U PANCHAPAKESAN1
1Renal Research Group, Kolling Institute, Royal North Shore Hospital, University of Sydney, Sydney, Australia

Aim: To assess if primary cilial Protein#1 is regulated by transforming growth factor beta (TGFB1) and evaluate if gene-silencing with sequence-specific LNA GapmeRs (Exiqon) affect downstream markers of kidney fibrosis.
Background: Primary cilia on kidney proximal tubule cells (PTCs) are sensitive to luminal mechanosensory stimuli and are a novel pathway linking luminal changes with tubular dysfunction. Our target, primary cilia Protein#1, is integral to the hedgehog signalling pathway, hence relevant to kidney fibrosis.
Methods: Primary cultures of mice PTC and human kidney (HK2) cells were transfected using control and Protein#1-sequence-specific LNA GapmeRs. Mice PTCs and HK2 cells were exposed to 5 or 2 ng/ml TGFB1 respectively for 48h. Kidney tissue from control and mice with streptozotocin-induced diabetes mellitus was harvested. mRNA expression of Protein#1 and downstream profibrotic markers were assessed.
Results: Protein#1 was upregulated in kidneys of diabetic mice (N=10-12,P<0.001) and HK2 cells (N=4,P<0.05) exposed to TGFB1 for 48h. A similar trend was seen in mice PTCs exposed to TGFB (N=4,P=0.08).Mice PTCs exposed to TGFB upregulated fibronectin (N=4,P<0.05) and collagen1 (N=3,P<0.05). Silencing of Protein#1 using sequence-specific LNA GapmeRs reduced expression of collagen1 (N=3,P<0.05), with a similar trend observed for fibronectin (N=4,P<0.06).HK2 cells exposed to TGFB upregulated collagen 4 (N=4,P<0.05), plasminogen activator inhibitor (PAI) (N=4,P=0.01) with a similar  trend observed for fibronectin (N=4,P=0.08). Silencing of Protein#1-as above reduced fibronectin (N=4,P<0.01) and  PAI (N=4,P<0.001). A similar trend was observed for collagen 4 expression (N=4,P=0.06).
Conclusion: Primary cilia Protein#1 is upregulated in mice diabetic kidneys and in TGFB1-exposed HK2 cells. Gene-silencing with Protein#1-sequence-specific LNA GapmeR reduced downstream markers of kidney fibrosis, suggesting its involvement in kidney fibrosis thus suggesting Protein#1 is a potential therapeutic target.


Biography:
Sanela Redzepagic is a nephrologist from Sydney. She is undertaking a PhD candidature at The University of Sydney, with Prof. Pollock’s Renal Research Lab, Koling Institute – Royal North Shore Hospital, to investigate a role of LNCRNA in the DKD

COMBINED PARICALCITOL AND ENALAPRIL IMPROVES HYPERTENSION BUT NOT KIDNEY CYST GROWTH IN EXPERIMENTAL POLYCYSTIC KIDNEY DISEASE

P SAGAR1,2, J ZHANG1,2, C MANNIX1,2, AT WONG1,2, G RANGAN1,2
1Centre for Transplant and Renal Research, Westmead Institute of Medical Research, University of Sydney, Sydney, Australia, 2Department of Renal Medicine, Westmead Hospital, Western Sydney Local Health District, Sydney, Australia

Aim: To determine the effect of paricalcitol (PC) on kidney cyst growth and hypertension in polycystic kidney disease (PKD).
Background: Vitamin D receptor agonists (VDRAs) reduce cell proliferation, hypertension and the renal activation of the renin-angiotensin system in chronic kidney diseases, but their role in PKD is not defined.
Methods: In Study 1, the preventative effects of monotherapy with PC on kidney cyst growth were assessed, and Lewis polycystic kidney disease (LPK) rats (a genetic ortholog of human nephronopthisis) received either PC (0.2 μg/kg/d by daily i.p.i) or vehicle (V) from weeks 3 to 10 (n=6 each). In Study 2, the therapeutic effects were assessed and LPK rats received either PC (0.8μg /kg by i.p.i. 3x/week), V, enalapril (E, 50 mg/L in drinking water) or a combination of E+PC from weeks 10 to 20 (n=5-7 each).
Results: In Study 1, PC did not reduce renal cyst growth or hypertension without adverse effects on serum calcium. In Study 2, the use of PC + E synergistically improved hypertension, more so than the effect of E alone, at both week 13 (LPK+V: 128+15; LPK+E: 103+17; LPK+PC: 137+11; LPK+PC+E: 100+6 mmHg, systolic blood pressure; P<0.01) and week 19 (LPK+V: 119+18; LPK+E: 117+12; LPK+P: 127+10; LPK+PC+E: 94+16 mmHg, systolic blood pressure, p<0.01). At week 20, this protective effect was associated with reduced cardiac enlargement (LPK+V: 0.45+0.03; LPK+E: 0.40+0.02; LPK+PC: 0.42+0.03; LPK+PC+E: 0.37+0.03; %cardiac:BW, p<0.01) but caused hypercalcaemia (LPK+V: 2.8+0.1; LPK+E: 2.8+0.0; LPK+PC: 3.6+0.03; LPK+PC+E: 3.4+0.3 mmol/L; p<0.01).
Conclusions: PC potentiates the anti-hypertensive action of ACE-inhibitors in experimental PKD but did not reduce renal cyst growth and resulted in significant hypercalcaemia. This cautions against further evaluation in clinical trials.


Biography:
Priyanka is a nephrology advanced trainee at Westmead training network and is interested in experimental and clinical research in polycystic kidney diseases. She is currently completing a MPhil (medical research) at Westmead Institute of Medical Research, University of Sydney.

SUBCLINICAL ACUTE KIDNEY INJURY (sAKI) MODIFIES BIOMARKER PROFILES IN SUBCLINICAL CHRONIC KIDNEY DISEASE (sCKD)

L SUCCAR1,  J WONG1, K TAYLOR1, A AU1, J ERLICH1, E ZOLTAN1
1University of New South Wales, Department of Nephrology, Prince of Wales Clinical School., Randwick, Sydney, Australia

Aim: To investigate biomarker profiles when ischaemic sAKI is superimposed on sCKD.
Background: sCKD (structural kidney damage without a rise in sCr) modifies diagnosis of nephrotoxin-induced AKI. Renal ischaemia in the presence of pre-existing sCKD may better reflect AKI in Australian adults.
Methods: sCKD was induced in Sprague Dawley rats by dietary supplementation with 0.25% adenine from day 0 to 28 or normal diet in controls. On day 56, sAKI was induced by brief duration renal ischaemic injury insufficient to induce sCr change in normal animals, viz bilateral clamping of the renal arteries for 30 minutes. sCr, urinary biomarkers (kidney injury molecule-1 (KIM-1), monocyte chemotactic protein 1 (MCP-1), clusterin, and interleukin-18 (IL-18)) and histological damage were measured after 1, 2, 3, 7 and 14 days.
Results: During induction of sCKD, urinary biomarker levels increased from day 3 to 21 and returned to baseline by day 56, despite absence of sCr rise. Rats displayed widespread medullary and up to 50% cortical damage. After sAKI in control rats, sCr did not increase and only KIM-1 rose from day 1 to 3 with focal medullary structural damage that recovered by day 7. In sCKD rats, all urinary biomarkers increased from day 1 to 7 post sAKI, and sCr increased continuously until day 14. Severe diffuse structural damage was also present from  day 1 after sAKI and persisted until 14 days.
Conclusions: Biomarker profiles are modified after sAKI is superimposed on sCKD. This impacts interpretation of AKI biomarker thresholds since sCKD in Australian adults is likely common and precursory to overt CKD.


Biography:
Dr Lena Succar is a Postdoctoral Research Fellow at the Prince of Wales Clinical School University of New South Wales, headed by Professor Zoltan Endre. Dr Succar’s research interest is centred on discovery of novel biomarker for early detection and profiling in CKD pathogenesis and progression, particular, in subclinical CKD (Which most likely reflects the adult population) and its modification after AKI.

VALIDATION OF NON-INVASIVE TRANSCUTANEOUS METHOD FOR GLOMERULAR FILTRATION RATE (GFR) IN OBESE MICE

T MULLINS1,2, W SHENG TAN1, L GALLO1,2
1School Of Biomedical Sciences, The University of Queensland, St Lucia, Australia, 2Mater Research Institute-UQ, Translational Research Institute, Woollongabba, Australia

Aim: To validate a non-invasive transcutaneous method for assessing glomerular filtration rate (GFR) in obese mice.
Background: The measurement of GFR in experimental rodents is pivotal to understanding the progression of kidney disease and the benefits of treatment strategies. Traditional methods can be invasive, inaccurate, and/or labour-intensive. This has led to development of a non-invasive clearance device (NIC-Kidney), which measures transcutaneous decay of injected FITC-sinistrin in conscious rodents. The technique has been tested and used in a range of mouse models. However, simultaneous comparisons to an established method have not been performed, and the technique is yet to be validated in obese mice.
Methods: Five-week-old male C57BL/6J mice were randomised to either a high fat diet (60% kcal from fat, n=13) or normal diet (n=12) for 10 weeks. Body composition was measured using NMR mini-spec. Mice were subjected to a single retro-orbital injection of FITC-sinistrin (10mg/100g) and transcutaneous decay using the NIC-Kidney Device was simultaneously compared to plasma clearance (two-phase exponential decay) in the same, conscious mice.
Results: Mice randomised to high fat vs normal diet developed obesity (BW: 32.2 vs 26.6 g, fat mass: 23 vs 14%, P<0.01). In lean mice, there was a linear relationship between transcutaneous and plasma clearance GFR values (linear regression: P<0.05, R2 = 0.35), which remained when GFR was adjusted for body weight (linear regression: P<0.01, R2 = 0.48). This relationship between GFR values, using the two methods, was not evident in obese mice.
Conclusions: The non-invasive transcutaneous method for assessing GFR is suitable for use in lean, but not obese, mice. This may be due to impairments in cutaneous blood flow in obesity, which requires study.


Biography:
Thomas Mullins completed a Bachelor of Science (First Class Honours) at The University of Queensland in 2017. His current research interests include diabetic nephropathy, anti-diabetic therapies that target the kidneys (SGLT2 inhibitors), and diabetes complications in pregnancy. Thomas is enrolled to commence a PhD project at The University of Queensland in the next academic quarter, supervised by Dr Helen Barrett, Dr Linda Gallo and Prof Karen Moritz. His PhD will focus on pregnancies complicated by type 2 diabetes mellitus, and associations of the microbiome with pregnancy and infant outcomes.

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