ORCID Profile
0000-0001-5763-095X
Current Organisations
Nepean Blue Mountains Local Health District
,
Royal Australasian College of Physicians
,
University of Sydney
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Publisher: Human Kinetics
Date: 08-2017
Abstract: Poor cardiorespiratory fitness is associated with increased all cause morbidity and mortality. In children with obesity, maximum oxygen uptake (V̇O 2max ) may not be achieved due to reduced motivation and peripheral fatigue. We aimed to identify a valid submaximal surrogate for V̇O 2max in children with obesity. Ninety-two children with obesity (7–16 years) completed a maximal exercise treadmill test and entered a three-month exercise and/or nutrition intervention after which the exercise test was repeated ( n = 63). Participants were required to reach V̇O 2max to be included in this analysis ( n = 32 at baseline and n = 13 at both time-points). The oxygen uptake efficiency slope (OUES) was determined as the slope of the line when V̇O 2 (L/min) was plotted against log V̇E. Associations between the maximal OUES, submaximal OUES (at 3, 4, 5 and 6 min of the exercise test) and V̇O 2max were calculated. In the cross-sectional analysis, V̇O 2max (L/min) was strongly correlated with 5-min OUES independent of Tanner puberty stage and sex ( R 2 = .80, p .001). Longitudinal changes in V̇O 2max were closely reflected by changes in 5-min OUES independent of change in percent body fat ( R 2 = .63, p .05). The 5-min OUES is a viable alternative to V̇O 2max when assessing children with obesity.
Publisher: Wiley
Date: 21-12-2015
DOI: 10.1111/TRA.12342
Publisher: Wiley
Date: 02-1987
DOI: 10.1111/J.1479-828X.1987.TB00930.X
Abstract: Eighty-seven infants (0.13% of livebirths) developed necrotizing enterocolitis (NEC) during a 15-year period at the Mercy Maternity Hospital, Melbourne. The disease was associated with 23 deaths, representing a mortality rate of 26.4% and comprising 2.6% of all neonatal deaths. The incidence of NEC increased from 0.07% of all livebirths for the years 1971-1974 to 0.25% for the 19-month period from January, 1984 to July, 1985. The mean age at onset was 9.9 days with an inverse relationship between birth-weight and age of onset of the disease. The mothers of the infants who developed NEC belonged to a significantly higher risk obstetric population gestational diabetes was identified in 3 of 28 mothers (10.6%) having glucose tolerance tested, and 1 other patients was a known diabetic. Subnormal oestriol excretion was detected in 15 of 45 patients tested, treble the overall hospital incidence. Of the 87 infants, 26 (29.9%) were VLBW (birth-weight less than 1,500 g), 5 were term (5.7%) and 9 (10.3%) were small for gestational age. The mean gestational age was 34.7 weeks and mean birth-weight was 1,988 g. Sixty-seven (77%) infants received medical treatment alone and 20 (23%) also received surgical treatment. Sequelae which developed in survivors were colonic strictures (4), fistulas (2) and the short-gut syndrome (1).
Publisher: Elsevier BV
Date: 03-2003
Publisher: Wiley
Date: 29-04-2015
DOI: 10.1111/TRA.12282
Publisher: Hindawi Limited
Date: 03-11-2019
DOI: 10.1155/2019/2193723
Abstract: Background . Increased visceral adipose tissue (VAT) is strongly associated with cardiometabolic risk factors. Accurate quantification of VAT is available through magnetic resonance imaging (MRI), which incurs a significant financial and time burden. We aimed to assess the accuracy of dual-energy X-ray absorptiometry- (DXA-) derived VAT (DXA-VAT) against a gold standard MRI protocol (MRI-VAT) in children with normal weight and obesity cross-sectionally, and over the course of a lifestyle intervention. Methodology . MRI-VAT and DXA-VAT were quantified in 61 children (30 normal weight and 31 with obesity) at baseline. Children with obesity entered a three-month exercise and/or nutrition intervention after which VAT was reassessed. MRI- and DXA-VAT cross-sectional area, volume, and mass were quantified, and associations were calculated at baseline ( n = 61) and pre-post intervention ( n = 28, 3 participants dropped out). Method agreement was assessed through Bland–Altman analysis, linear regression, and Passing–Bablok regression. Results . At baseline, all DXA- and MRI-VAT outcomes were strongly associated ( r = 0.90, P 0.001 ). However, there were no significant associations between absolute or relative change in DXA- and MRI-VAT outcomes ( r = 0.25–0.36, P 0.05 ). DXA significantly overestimated VAT CSA (cross-sectional area), volume, and mass when compared with MRI ( P 0.001 ) at baseline. Significant proportional bias was observed for all DXA-VAT outcomes at baseline and for relative longitudinal changes in DXA-VAT. Conclusions . Although DXA-VAT outcomes were strongly associated with MRI-VAT outcomes at baseline, estimates were subject to proportional bias in children with obesity and normal weight. DXA lacks validity for detecting changes in VAT among children with obesity. This trial is registered with NCT01991106 .
Publisher: The Endocrine Society
Date: 12-2010
DOI: 10.1210/JC.2010-0647
Abstract: Introduction: It has been postulated that central adrenal insufficiency (CAI), resulting from hypothalamic dysfunction, may contribute to the increased unexplained death rates in Prader Willi syndrome (PWS). A study using the overnight metyrapone test reported a 60% prevalence of CAI in children with PWS. We used a low-dose Synacthen test to screen for CAI in children with PWS. Methods: We studied 41 children with genetic diagnosis of PWS [20 males mean age, 7.68 (±5.23) yr] in five pediatric endocrinology centers in Australasia. All participants were randomly selected, and none had a history of Addisonian crisis. Ten of the cohort were receiving sex hormone therapy, 19 were receiving GH, and four were receiving T4. Their mean body mass index z-score was +1.48 (±1.68). Baseline morning ACTH and cortisol levels were measured, followed by iv administration of 1 μg Synacthen. Post-Synacthen cortisol levels were measured at 30 min, and a cortisol level above 500 nmol/liter was considered normal. Results: The mean baseline ACTH and cortisol were 15 (±14) ng/liter and 223 (±116) nmol/liter, respectively. The mean 30-min plasma cortisol was 690 (±114) nmol/liter, and the average increase from baseline was 201%. Conclusions: Our result suggests that CAI is rare in children with PWS.
Publisher: The Endocrine Society
Date: 1995
DOI: 10.1210/JC.80.1.320
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2016
Publisher: Walter de Gruyter GmbH
Date: 2021
Abstract: Adolescence is a challenging period for diabetes management, particularly when transitioning to adult care. There are reports highlighting concerns that transition to adult care may lead to poor glycemic control and clinic engagement. Our aim was to determine if a co-located pediatric and transition diabetes service would lead to better transition outcomes. A retrospective medical records review was conducted on patients with type 1 diabetes attending a transition clinic in a metropolitan teaching hospital in Sydney, Australia. Patients referred from the hospital’s co-located pediatric diabetes clinic to the transition clinic were compared to those referred from external sources regarding important clinical outcomes such as glycosylated haemoglobin (HbA 1c ), clinic attendances, and complication rates between referral sources. Confounders such as age, gender, duration of diabetes and socioeconomic status were considered. Data was collected from 356 patients of which 121 patients were referred from the co-located pediatric diabetes clinic (IRG) and 235 patients from external sources (ERG). Improvements in HbA 1c were only seen in the ERG at 6 and 12 months (p .001). Altogether 93% attended one or more medical appointments in the IRG compared to 83% in the ERG (p=0.03). There were more admissions for acute diabetes complications (17 vs. 8%, p=0.01) and more microvascular complications (20 vs. 9%, p .01) in the IRG vs. ERG group. Although co-location of a pediatric and transition clinic improved medical engagement, this did not equate to better glycemic control or complication rates. Further research is warranted to determine what other strategies are required to optimise the transition process in diabetes care.
Publisher: Wiley
Date: 24-08-2020
DOI: 10.1111/COB.12391
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2016
Publisher: Wiley
Date: 2007
DOI: 10.1359/JBMR.061010
Abstract: The long-term effects on bone and fat mass in children with endogenous CS are unknown. In 14 children followed for 3-7 years into young adulthood after cure of CS, whereas bone mass largely recovered, persisting increases in total body and visceral fat suggests an increase risk of the metabolic syndrome. Endogenous Cushing syndrome (CS) is associated with decreased bone mass and increased central fat mass. Whereas bone mass seems to improve after successful treatment, little is known about whether central fat persists. This was a prospective study of 14 children (10 girls and 4 boys) and adolescents with CS who were successfully treated and remained eucortisolemic. Growth, puberty, bone mass, and body composition were evaluated at baseline and during regular follow-up for 3 years and in seven children for a further 4 years of remission to assess final adult height (FH), BMI, bone mass, and body composition. CS compromised growth, leading to about a -0.8 SD loss of FH and 0.9 SD increase in weight and BMI. BMD apparent density (BMAD) SD Score (SDS) at the lumbar spine (LS) at diagnosis were -1.8 and -1.25, respectively, and after 3 years of follow-up approached the mean with no further increase apparent up to 7 years of follow-up. Whereas hip BMD SDS increased from -1.3 at diagnosis to -0.40 at 3 years and 0 at 7 years of follow-up, femoral neck BMAD remained at or around 0 SDS at diagnosis and during follow-up. BMI was >25 kg/m(2) in five of seven adult subjects, most of whom were women. Total body fat and the ratio of visceral to subcutaneous was abnormally high in the majority of these subjects, whereas LS volumetric BMD was -0.7 SDS. Despite remission of CS, children and adolescents have significant alterations in body composition that result in a small but significant decrease in bone mass and increase in visceral adiposity. Although bone mass largely recovers after endogenous CS, changes in total and visceral fat suggest these subjects are at increased risk of the metabolic syndrome. Therefore, long-term monitoring of body fat and bone mass is mandatory after treatment of CS.
Publisher: The Endocrine Society
Date: 12-2004
DOI: 10.1210/EN.2004-0061
Abstract: Suppressors of cytokine signaling (SOCS) are important negative regulators of cytokine action. We recently reported that estrogen stimulates SOCS-2 expression and inhibits GH signaling in kidney cells. The effects of estrogen on SOCS expression in other tissues are unclear. The aim of this study was to investigate in vivo and in vitro whether estrogen affected SOCS expression in the liver, a major target organ of GH. The in vivo hepatic effects of estrogen on ovariectomized mice lacking estrogen receptor (ER)-α, ERβ, or both and their wild-type littermates were examined by DNA microarray analysis. In vitro, the effects of estrogen on SOCS expression in human hepatoma cells were examined by reverse transcription quantitative PCR. Long-term (3 wk) estrogen treatment induced a 2- to 3-fold increase in hepatic expression of SOCS-2 and -3 in wild-type and ERβ knockout mice but not in those lacking ERα or both ER subtypes. Short-term treatment (at 24 h) increased the mRNA level of SOCS-3 but not SOCS-2. In cultured hepatoma cells, estrogen increased SOCS-2 and -3 mRNA levels by 2-fold in a time- and dose-dependent manner (P & 0.05). Estrogen induced murine SOCS-3 promoter activity by 2-fold (P & 0.05) in constructs containing a region between nucleotides −1862 and −855. Moreover, estrogen and GH had additive effects on the SOCS-3 promoter activity. In summary, estrogen, via ERα, up-regulated hepatic expression of SOCS-2 and -3, probably through transcriptional activation. This indicates a novel mechanism of estrogen regulation of cytokine action.
Publisher: The Royal Australian College of General Practitioners
Date: 07-2023
Publisher: Elsevier BV
Date: 05-2001
Publisher: Hindawi Limited
Date: 02-2009
DOI: 10.1111/J.1399-5448.2008.00439.X
Abstract: There is considerable evidence supporting the role of vitamin D deficiency in the pathogenesis of type 1 diabetes mellitus (T1DM). Vitamin D deficiency is also associated with impairment of insulin synthesis and secretion. There have been no formal studies looking at the relationship between 25(OH)-vitamin D(3) and the severity of diabetic ketoacidosis (DKA) in children at presentation with T1DM. To determine the relationship between measured 25(OH)-vitamin D(3) levels and the degree of acidosis in children at diagnosis with T1DM. Children presenting with new-onset T1DM at a tertiary children's hospital. 25(OH)-vitamin D(3) and bicarbonate levels were measured in children at presentation with newly diagnosed T1DM. Those with suboptimal 25(OH)-vitamin D(3) levels (<50 nmol/L) had repeat measurements performed without interim vitamin D supplementation. Fourteen of the 64 children had low 25(OH)-vitamin D(3) levels at presentation, and 12 of these had low bicarbonate levels (<18 mmol/L) (p = 0.001). Bicarbonate explained 20% of the variation in vitamin D level at presentation (partial r(2) = 0.20, p < 0.001) and ethnic background a further 10% (partial r(2) = 0.10, p = 0.002). The levels of 25(OH)-vitamin D(3) increased in 10 of the 11 children with resolution of the acidosis. Acid-base status should be considered when interpreting 25(OH)-vitamin D(3) levels in patients with recently diagnosed T1DM. Acidosis may alter vitamin D metabolism, or alternatively, low vitamin D may contribute to a child's risk of presenting with DKA.
Publisher: Elsevier BV
Date: 05-2019
Publisher: Elsevier BV
Date: 04-0001
DOI: 10.1016/J.MCE.2022.111570
Abstract: Complete androgen insensitivity syndrome (CAIS), where 46,XY in iduals present as female, is caused by variants in the androgen receptor gene (AR). We analyzed the DNA of a patient with suspected CAIS using a targeted gene sequencing panel and whole exome sequencing (WES) but did not detect any small nucleotide variants in AR. Analysis of WES data using our bioinformatics pipeline designed to detect copy number variations (CNV) uncovered a rare duplication of exon 2 of AR. Using array comparative genomic hybridization, the duplication was found to span 43.6 kb and is predicted to cause a frameshift and loss of AR protein. We confirmed the power of our WES-CNV detection protocol by identifying pathogenic CNVs in FSHR and NR5A1 in previously undiagnosed patients with disorders of sex development. Our findings illustrate the usefulness of CNV analysis in WES data to detect pathogenic genomic changes that may go undetected using only standard analysis protocols.
Publisher: Elsevier BV
Date: 05-2001
Start Date: 2004
End Date: 2006
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2004
End Date: 2006
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2008
End Date: 2010
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2006
End Date: 2011
Funder: National Health and Medical Research Council
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