ORCID Profile
0000-0002-2914-8012
Current Organisations
University of Western Australia
,
Curtin University Curtin Medical School
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Publisher: Cold Spring Harbor Laboratory
Date: 24-07-2023
DOI: 10.1101/2023.07.20.23292940
Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial pneumonia marked by progressive lung fibrosis and a poor prognosis. Recent studies have highlighted the potential role of infection in the pathogenesis of IPF and a prior association of the HLA-DQB1 gene with idiopathic fibrotic interstitial pneumonia (including IPF) has been reported. Due to the important role that the Human Leukocyte Antigen (HLA) region plays in the immune response, here we evaluated if HLA genetic variation was associated specifically with IPF risk. We performed a meta-analysis of associations of the HLA region with IPF risk in in iduals of European ancestry from seven independent case-control studies of IPF (comprising a total of 5,159 cases and 27,459 controls, including the prior study of fibrotic interstitial pneumonia). Single nucleotide polymorphisms, classical HLA alleles and amino acids were analysed and signals meeting a region-wide association threshold p .5×10 −4 and a posterior probability of replication % were considered significant. We sought to replicate the previously reported HLA-DQB1 association in the subset of studies independent of the original report. The meta-analysis of all seven studies identified four significant independent single nucleotide polymorphisms associated with IPF risk. However, none met the posterior probability for replication criterion. The HLA-DQB1 association was not replicated in the independent IPF studies. Variation in the HLA region was not consistently associated with risk in studies of IPF. However, this does not preclude the possibility that other genomic regions linked to the immune response may be involved in the aetiology of IPF.
Publisher: Wiley
Date: 30-11-2019
DOI: 10.1111/RESP.13451
Abstract: Bronchiectasis is a chronic lung disease associated with structurally abnormal bronchi, clinically manifested by a persistent wet roductive cough, airway infections and recurrent exacerbations. Early identification and treatment of acute exacerbations is an integral part of monitoring and annual review, in both adults and children, to minimize further damage due to infection and inflammation. Common modalities used to monitor disease progression include clinical signs and symptoms, frequency of exacerbations and/or number of hospital admissions, lung function (forced expiratory volume in 1 s (FEV
Publisher: European Respiratory Society (ERS)
Date: 21-10-2021
DOI: 10.1183/13993003.01181-2021
Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease in which circulatory biomarkers have the potential for guiding management in clinical practice. We assessed the prognostic role of serum biomarkers in three independent IPF cohorts: Australian Idiopathic Pulmonary Fibrosis Registry (AIPFR), Trent Lung Fibrosis (TLF) and Prospective Observation of Fibrosis in the Lung Clinical Endpoints (PROFILE). In the AIPFR cohort, candidate proteins were assessed by ELISA as well as in an unbiased proteomic approach. LASSO (least absolute shrinkage and selection operator) regression was used to restrict the selection of markers that best accounted for the progressor phenotype at 1 year in the AIPFR cohort, and subsequently prospectively selected for replication in the validation TLF cohort and assessed retrospectively in the PROFILE cohort. Four significantly replicating biomarkers were aggregated into a progression index model based on tertiles of circulating concentrations. 189 participants were included in the AIPFR cohort, 205 participants from the TLF cohort and 122 participants from the PROFILE cohort. Differential biomarker expression was observed by ELISA and replicated for osteopontin, matrix metallopeptidase-7, intercellular adhesion molecule-1 and periostin for those with a progressor phenotype at 1 year. Proteomic data did not replicate. The progression index in the AIPFR, TLF and PROFILE cohorts predicted risk of progression, mortality and progression-free survival. A statistical model incorporating the progression index demonstrated the capacity to distinguish disease progression at 12 months, which was increased beyond the clinical GAP (gender, age and physiology) score model alone in all cohorts, and significantly so within the incidence-based TLF and PROFILE cohorts. A panel of circulatory biomarkers can provide potentially valuable clinical assistance in the prognosis of IPF patients.
Publisher: American Thoracic Society
Date: 05-2018
Publisher: Elsevier BV
Date: 09-2011
DOI: 10.1016/J.RMED.2011.05.008
Abstract: To ascertain the trends in mortality from Asbestosis, Extrinsic Allergic Alveolitis (EAA) and Sarcoidosis in England and Wales, we analysed mortality data from the Office of National Statistics. We calculated age and stratum specific mortality rates between 1968 and 2008 and applied these to the 2008 population to generate annual standardised expected number of deaths. Poisson regression was used to calculate annual mortality rate ratios. From 1968 to 2008 there were 1958 registered deaths from Asbestosis, 878 deaths from EAA and 3544 deaths from Sarcoidosis. The Asbestosis mortality rate increased from 0.04 (95% CI 0.03-0.05) in the 1968-1972 calendar period to 0.12 (95% CI 0.10-0.13) in the 2005-2008 period whist the mortality from EAA increased marginally from 0.04 (95% CI 0.03-0.05) in the 1968-1972 calendar period to 0.08 (95% CI 0.07-0.09) in the 2005-2008 period. Mortality from Sarcoidosis increased by approximately 9% a year. Our findings show that the mortality from Asbestosis continues to rise in the UK. Overall mortality rates from EAA remained stable throughout the same period but it was higher in males and in older people. There was a slight increase in mortality from Sarcoidosis over the study period which was greater in women.
Publisher: European Respiratory Society (ERS)
Date: 22-09-2016
DOI: 10.1183/13993003.00378-2016
Abstract: International guidelines and new targeted therapies for idiopathic pulmonary fibrosis have increased the need for accurate diagnosis of interstitial lung disease (ILD), which may lead to more surgical lung biopsies. This study aimed to assess the risk of this procedure in patients from the UK. We used Hospital Episodes Statistics data from 1997 to 2008 to assess the frequency of surgical lung biopsy for ILD in England, UK. We identified cardiothoracic surgical patients using International Classification of Diseases revision 10 codes for ILD and Office of Population Censuses and Surveys Classification of Interventions and Procedures version 4 codes for surgical lung biopsy. We excluded those with lung resections or lung cancer. We estimated in-hospital, 30-day and 90-day mortality following the procedure, and linked to cause of death using data from the UK Office of National Statistics. We identified 2820 patients with ILD undergoing surgical lung biopsy during the 12-year period. The number of biopsies increased over the time period studied. In-hospital, 30-day and 90-day mortality were 1.7%, 2.4% and 3.9%, respectively. Male sex, increasing age, increasing comorbidity and open surgery were risk factors for mortality. Surgical lung biopsy for ILD has a similar mortality to lobectomy for lung cancer, and clinicians and patients should understand the likely risks involved.
Publisher: European Respiratory Society (ERS)
Date: 31-01-2015
Publisher: American Thoracic Society
Date: 10-2014
Publisher: Cold Spring Harbor Laboratory
Date: 30-03-2022
DOI: 10.1101/2022.03.28.22272832
Abstract: Idiopathic pulmonary fibrosis (IPF) is an incurable disease characterised by progressive scarring of the lungs. This leads to the lungs becoming stiffer, reducing lung capacity, and impeding gas transfer. We aimed to identify genetic variants associated with either declining lung capacity or gas transfer after diagnosis of IPF. We performed a genome-wide meta-analysis of longitudinal measures of forced vital capacity (FVC) and diffusing capacity for lung of carbon monoxide (DLco) in in iduals diagnosed with IPF from three studies. Suggestively significant variants were investigated further in an additional study. Variants were defined as significantly associated if they had a meta-analysis p ×10 −8 , had consistent direction of effects across all studies and were nominally significant (p .05) in each study. 1,048 in iduals with measures of longitudinal FVC and 729 in iduals with longitudinal measures of DLco passed quality control. In total, 4,560 measures of FVC and 2,795 measures of DLco and over 7 million genetic variants were included in the analysis. One variant located in an antisense RNA gene for Protein Kinase N2 ( PKN2 ) showed a genome-wide significant association with FVC decline (−140 ml/year per risk allele, 95% CI [−180, −100], p=9.14×10 −12 ). These results identify a possible druggable target involved in promoting IPF disease progression. Action for Pulmonary Fibrosis, Medical Research Council, Wellcome Trust, National Institute of Health/National Heart, Lung and Blood Institute Idiopathic pulmonary fibrosis (IPF) is a devastating disease where the lungs become scarred, this scarring leads to a reduced lung capacity, poorer rates of gas transfer and is eventually fatal. However, disease progression is highly variable and it is not clear why this is. To date, genome-wide association studies (GWAS) have identified 20 genetic loci associated with susceptibility to IPF. These genetic loci implicate genes involved with host defence, regulation of TGFβ signalling, telomere maintenance, cell-cell adhesion and spindle assembly as important biological processes involved in the pathogenesis of IPF. The GWAS variant with the strongest effect on disease risk is found in the promoter region of the MUC5B gene (rs35705950). Generally, the variants associated with IPF susceptibility show little or no association with disease progression, apart from the risk allele at rs35705950 which has been reported as having an association with improved survival times. Although genetic variants associated with disease risk have been widely studied, little has been reported to investigate the effect of genetics on progression of IPF. Here we present a GWAS of progressive IPF by identifying genetic variants associated longitudinal measures of lung health after diagnosis of IPF. We identify a genetic locus associated with a more rapid decline in lung capacity that lies in the RNA antisense gene of PKN2 . The novel genetic locus associated with a more rapid decline in lung capacity in in iduals with IPF implicates a Rho/RAC effector protein. Effective treatments for IPF are desperately needed. There are currently PKN2 inhibitors under development meaning this analysis highlights a potential therapeutic target for IPF. We also show the genetic determinants of IPF progression appear to be distinct from those that drive IPF susceptibility.
Publisher: Wiley
Date: 02-2021
DOI: 10.1111/IMJ.15191
Publisher: BMJ
Date: 27-04-2011
Abstract: Previous studies have shown that the incidence of idiopathic pulmonary fibrosis (IPF) is rising in the U.K. and U.S.A. Death registrations and primary care data were used to determine the current trends in IPF incidence in the U.K. Because routine clinical data sets were used, the term IPF clinical syndrome (IPF-CS) is used to describe in iduals in this study. Age- and stratum-specific death registration rates between 1968 and 2008 were calculated and these were applied to the 2008 population to generate annual standardised expected number of deaths. Annual mortality rate ratios were calculated using Poisson regression. Computerised primary care records were used to determine incidence rates of IPF-CS between 2000 and 2008 stratified by age, sex and geographical region, and survival rates between calendar periods were compared. Annual death certificate recording of IPF-CS rose sixfold across the study period from 0.92 per 100,000 in the 1968-1972 calendar periods to 5.10 per 100,000 in the 2006-2008 calendar period, and were higher in men and the older age groups. The incidence of IPF-CS in primary care increased by 35% from 2000 to 2008, with an overall incidence rate of 7.44 per 100,000 person-years (95% CI 7.12 to 7.77). Incidence was higher in men, the older population and in Northwest England. The incidence of IPF-CS in primary care and registered deaths from this cause in the U.K. continues to rise in the 21st century. The current findings suggest that there are >5000 new cases diagnosed each year in the U.K.
Publisher: American Thoracic Society
Date: 03-2020
Publisher: Elsevier BV
Date: 2023
Publisher: Elsevier BV
Date: 12-2011
DOI: 10.1016/J.RMED.2011.08.015
Abstract: Previous studies into the survival differences between in iduals with idiopathic pulmonary fibrosis and those with connective tissue disease associated pulmonary fibrosis (CTD-PF) have yielded mixed results. The aim of this study is to compare the survival of in iduals with CTD-PF to those with idiopathic pulmonary fibrosis clinical syndrome (IPF-CS) using data derived from The Health Improvement network, a large primary care database in the UK. Incident cases of CTD-PF and IPF-CS between the years 2000-2009 were identified. Survival analysis was performed using Kaplan-Meier methods, stratified by type of connective tissue disease. Cox regression was then used to compare mortality rates between the groups, adjusting for age, gender and year of diagnosis. A total of 324 cases of CTD-PF and 2209 cases of IPF-CS were followed up over a mean period of 2.3 years. During this period, 113 (34.9%) cases of CTD-PF and 1073 (48.6%) cases of IPF-CS died. The mortality rates for cases with CTD-PF and IPF-CS were 123.6 per 1000 person years (95%CI: 102.8-148.9) and 229.8 per 1000 person years (95% CI: 216.4-244.0) respectively. After adjusting for age, sex and year of diagnosis, cases with CTD-PF had a better prognosis compared to those with IPF-CS (HR 0.76,95%CI: 0.62-0.92). The prognosis of in iduals with CTD-PF appears to be significantly better than those with IPF-CS, but remains an important cause of death in patients with connective tissue disease, and requires more effective treatment options.
Publisher: European Respiratory Society (ERS)
Date: 16-10-2014
Publisher: European Respiratory Society
Date: 2016
Publisher: BMJ
Date: 29-01-2019
DOI: 10.1136/THORAXJNL-2018-212514
Abstract: Chronic respiratory diseases (CRD) are common, are increasing in prevalence, and cause significant morbidity and mortality worldwide. However, we have limited knowledge on causes of death of patients with CRD in the general population. We evaluated mortality rates and causes of death over time in patients with CRD. We used linked primary care and mortality data to determine mortality rates and the most common causes of death in people with CRD (including asthma, bronchiectasis, COPD and interstitial lung diseases (ILD)) during 2005–2015 in England. We identified 558 888 patients with CRD (451 830 asthma, 137 709 COPD, 19 374 bronchiectasis, 10 745 ILD). The age-standardised mortality rate of patients with CRD was 1607 per 100 000 persons (asthma=856, COPD=1503, ILD=2609, bronchiectasis=1463). CRD mortality was overall 54% higher than the general population. A third of patients with CRD died from respiratory-related causes. Respiratory-related mortality was constant, while cardiovascular-related mortality decreased significantly over time. COPD accounted for the majority of respiratory-related deaths (66% overall) in all patient groups except ILD. Patients with CRD continue to experience substantial morbidity and mortality due to respiratory diseases. Disease-modifying intervention strategies are needed to improve outcomes for patients with CRD.
Publisher: Cold Spring Harbor Laboratory
Date: 14-05-2019
DOI: 10.1101/636761
Abstract: Idiopathic pulmonary fibrosis (IPF) is a complex lung disease characterised by scarring of the lung that is believed to result from an atypical response to injury of the epithelium. The mechanisms by which this arises are poorly understood and it is likely that multiple pathways are involved. The strongest genetic association with IPF is a variant in the promoter of MUC5B where each copy of the risk allele confers a five-fold risk of disease. However, genome-wide association studies have reported additional signals of association implicating multiple pathways including host defence, telomere maintenance, signalling and cell-cell adhesion. To improve our understanding of mechanisms that increase IPF susceptibility by identifying previously unreported genetic associations. We performed the largest genome-wide association study undertaken for IPF susceptibility with a discovery stage comprising up to 2,668 IPF cases and 8,591 controls with replication in an additional 1,467 IPF cases and 11,874 controls. Polygenic risk scores were used to assess the collective effect of variants not reported as associated with IPF. We identified and replicated three new genome-wide significant ( P ×10 -8 ) signals of association with IPF susceptibility (near KIF15, MAD1L1 and DEPTOR) and confirm associations at 11 previously reported loci. Polygenic risk score analyses showed that the combined effect of many thousands of as-yet unreported IPF risk variants contribute to IPF susceptibility. Novel association signals support the importance of mTOR signalling in lung fibrosis and suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.
Publisher: BMJ
Date: 20-07-2023
Publisher: BMJ
Date: 10-06-2022
DOI: 10.1136/THORAXJNL-2021-218577
Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic lung condition with poor survival times. We previously published a genome-wide meta-analysis of IPF risk across three studies with independent replication of associated variants in two additional studies. To maximise power and to generate more accurate effect size estimates, we performed a genome-wide meta-analysis across all five studies included in the previous IPF risk genome-wide association studies. We used the distribution of effect sizes across the five studies to assess the replicability of the results and identified five robust novel genetic association signals implicating mTOR (mammalian target of rapamycin) signalling, telomere maintenance and spindle assembly genes in IPF risk.
Publisher: Public Library of Science (PLoS)
Date: 31-03-2023
DOI: 10.1371/JOURNAL.PONE.0283110
Abstract: Fibrotic interstitial lung disease (ILD) includes a large group of conditions that lead to scarring of the lungs. The lack of available 5-level EuroQol 5D (EQ5D) data has limited the ability to conduct economic evaluations in ILD. The purpose of this study was to develop and validate a mapping algorithm that predicts EQ5D utilities from commonly collected pulmonary function measurements (forced vital capacity [FVC] and diffusing capacity of the lung for carbon monoxide [DLCO]) in fibrotic ILDs. EQ5D utility and pulmonary function measurements from the Canadian Registry for Pulmonary Fibrosis were included. Ordinary least squares (OLS), beta regression, two-part, and tobit models were used to map EQ5D utilities from FVC or DLCO. Model performance was assessed by comparing the predicted and observed utilities. Subgroup analyses were also conducted to test how well models performed across different patient characteristics. The models were then externally validated in the Australian Idiopathic Pulmonary Fibrosis Registry. The OLS model performed as well as other more complex models (root mean squared error: 0.17 for FVC and 0.16 for DLCO). As with the other models, the OLS algorithm performed well across the different subgroups (except for EQ5D utilities 0.5) and in the external validation cohort. We developed a mapping algorithm that predicts EQ5D utilities from FVC and DLCO, with the intent that this algorithm can be applied to clinical trial populations and real-world cohorts that have not prioritized collection of health-related utilities. The mapping algorithm can be used in future economic evaluations of potential ILD therapies.
Publisher: American Thoracic Society
Date: 15-07-2019
Publisher: Wiley
Date: 11-07-2023
DOI: 10.1111/RESP.14552
Abstract: Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia. Participants were recruited from the Australian IPF Registry ( n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression. Median (25th–75th percentiles) annual fine particulate matter ( .5 μm, PM 2.5 ) and nitrogen dioxide (NO 2 ) were 6.8 (5.7, 7.9) μg/m 3 and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m 3 increase in PM 2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO 2 . There was also no association between air pollution and rapid progression of IPF. Living near a major road and increased PM 2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low‐level concentrations of exposure.
Publisher: BMJ
Date: 11-10-2017
DOI: 10.1136/THORAXJNL-2017-210177
Abstract: Little is known about when symptoms of idiopathic pulmonary fibrosis first develop. We identified incident cases of idiopathic pulmonary fibrosis-clinical syndrome (IPF-CS) from a UK primary care database and assessed the frequency of consultations for common symptoms in the 5 years prior to diagnosis. 1671 cases were identified with 5 years of data prior to diagnosis. Breathlessness was the most common symptom, followed by cough. Cases were significantly more likely than controls to experience these symptoms (p .001), even 4–5 years before diagnosis (OR for breathlessness for this period 2.79, 95% CI 2.13 to 3.65). This suggests that some patients with IPF may be symptomatic for more than 5 years before diagnosis.
Publisher: Springer Science and Business Media LLC
Date: 26-12-2022
Publisher: Elsevier BV
Date: 04-2013
Abstract: The lack of mandatory clinical registries for idiopathic pulmonary fibrosis (IPF) has meant a reliance on routine clinical data to provide trends in disease incidence. Death certificate and primary care data suggest that the incidence of IPF has increased in the United Kingdom at a rate of approximately 5% per year, but due to possible concerns about the diagnostic validity of these clinical datasets, it is helpful also to analyze data from secondary care. We used national secondary care data to determine trends in hospital admissions for IPF clinical syndrome (IPF-CS) in England between 1998 and 2010. We obtained the annual number of hospital admissions for all National Health Service (NHS) hospital trusts in England for the International Classification of Diseases and Related Health Problems, 10th Revision codes J84.1 and J84.9 between 1998 and 2010. We calculated annual admission-rate ratios, adjusting for age and sex, using Poisson regression. We also investigated changes in age at admission and length of stay, and we estimated hospitalization costs. The number of hospital admissions from IPF-CS increased at an annual rate of approximately 5%, from 5,524 patients in 1998 to 9,525 patients in 2010, and was highest in men and the older population. Mean age at admission increased from 66 to 71 years, while length of stay decreased by 2.1 days during the same period. Hospital admissions for IPF-CS in England follow a similar trend to other data sources in the United Kingdom . This has resulted in escalating costs of inpatient care, which is a significant financial burden on health-care resources.
Publisher: BMJ
Date: 03-09-2013
DOI: 10.1136/THORAXJNL-2013-203740
Abstract: Laboratory studies suggest that the clotting cascade is activated in fibrotic lungs. Since humans vary in their tendency to clot due to a variety of inherited or acquired defects, we investigated whether a prothrombotic state increases the chance of developing idiopathic pulmonary fibrosis (IPF) and/or worsens the prognosis of IPF. We recruited 211 incident cases of IPF and 256 age- and sex-matched general population controls and collected data on medical history, medication, smoking habit, blood s les as well as lung function and high-resolution CT scans done as part of routine clinical care. A prothrombotic state was defined as the presence of at least one inherited or acquired clotting defect or marker of fibrinolytic dysfunction. We used logistic regression to quantify the association between a prothrombotic state and IPF adjusted for age, sex, smoking habit and highly sensitive C reactive protein. Cox regression was used to determine the influence of a prothrombotic state on survival. Cases were more than four times more likely than controls to have a prothrombotic state (OR 4.78, 95% CI 2.93 to 7.80 p<0.0001). Cases with a prothrombotic state were also likely to have more severe disease (forced vital capacity <70% predicted) at presentation (OR 10.79, 95% CI 2.43 to 47.91) and had a threefold increased risk of death (HR 3.26, 95% CI 1.09 to 9.75). People with IPF are more likely to have a prothrombotic state than general population controls and the presence of a prothrombotic state has an adverse impact on survival.
Publisher: American Thoracic Society
Date: 03-2018
Publisher: Elsevier BV
Date: 2015
Abstract: People with idiopathic pulmonary fibrosis (IPF) have been shown to be at an increased risk for cardiovascular (CV) disease, but reasons for this are unknown. The aim of this study was to compare the prevalence of common CV risk factors in people with IPF and the general population and establish the incidence of ischemic heart disease (IHD) and stroke after the diagnosis of IPF, controlling for these risk factors. We used data from a large, UK primary care database to identify incident cases of IPF and matched general-population control subjects. We compared the prevalence of risk factors for CV disease and prescription of CV medications in people with IPF (before diagnosis) with control subjects from the general population and assessed the incidence of IHD and stroke in people with IPF (after diagnosis) compared with control subjects. We identified 3,211 cases of IPF and 12,307 control subjects. Patients with IPF were more likely to have a record of hypertension (OR, 1.31 95% CI, 1.19-1.44), and diabetes (OR, 1.20 95% CI, 1.07-1.34) compared with control subjects they were also more likely to have been prescribed several CV drugs. The rate of first-time IHD events was more than twice as high in patients than control subjects (rate ratio, 2.32 95% CI, 1.85-2.93 P < .001), but the incidence of stroke was only marginally higher (P = .09). Rate ratios for IHD and stroke were not altered substantially after adjusting for CV risk factors. Several CV risk factors were more prevalent in people with IPF however, this did not account for the increased rate of IHD in this group of patients.
Publisher: Wiley
Date: 08-06-2016
DOI: 10.1111/BCP.12983
Publisher: Oxford University Press (OUP)
Date: 17-11-2015
DOI: 10.1093/QJMED/HCV206
Publisher: Springer Science and Business Media LLC
Date: 03-10-2014
Location: United Kingdom of Great Britain and Northern Ireland
Location: Australia
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Vidya Navaratnam.