ORCID Profile
0000-0002-6018-0547
Current Organisations
University of Western Australia
,
Sir Charles Gairdner Hospital
,
Hollywood Private Hospital
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Publisher: Wiley
Date: 21-11-2022
DOI: 10.1111/RESP.14414
Abstract: See related article
Publisher: Wiley
Date: 24-01-2023
DOI: 10.1111/RESP.14454
Publisher: American Thoracic Society
Date: 05-2021
Publisher: American Association for the Advancement of Science (AAAS)
Date: 02-09-2022
Abstract: In mice and humans with cancer, intravenous 13 C-glucose infusion results in 13 C labeling of tumor tricarboxylic acid (TCA) cycle intermediates, indicating that pyruvate oxidation in the TCA cycle occurs in tumors. The TCA cycle is usually coupled to the electron transport chain (ETC) because NADH generated by the cycle is reoxidized to NAD + by the ETC. However, 13 C labeling does not directly report ETC activity, and other pathways can oxidize NADH, so the ETC’s role in these labeling patterns is unverified. We examined the impact of the ETC complex I inhibitor IACS-010759 on tumor 13 C labeling. IACS-010759 suppresses TCA cycle labeling from glucose or lactate and increases labeling from glutamine. Cancer cells expressing yeast NADH dehydrogenase-1, which recycles NADH to NAD + independently of complex I, display normalized labeling when complex I is inhibited, indicating that cancer cell ETC activity regulates TCA cycle metabolism and 13 C labeling from multiple nutrients.
Publisher: Springer Science and Business Media LLC
Date: 11-08-2021
DOI: 10.1186/S12889-021-11578-Y
Abstract: Chronic medical conditions accumulate within in iduals with age. However, knowledge concerning the trends, patterns and determinants of multimorbidity remains limited. This study assessed the prevalence and patterns of multimorbidity using extensive in idual phenotyping in a general population of Australian middle-aged adults. Participants ( n = 5029, 55% female), born between 1946 and 1964 and attending the cross-sectional phase of the Busselton Healthy Ageing Study (BHAS) between 2010 and 2015, were studied. Prevalence of 21 chronic conditions was estimated using clinical measurement, validated instrument scores and/or self-reported doctor-diagnosis. Non-random patterns of multimorbidity were explored using observed/expected (O/E) prevalence ratios and latent class analysis (LCA). Variables associated with numbers of conditions and class of multimorbidity were investigated. The in idual prevalence of 21 chronic conditions ranged from 2 to 54% and multimorbidity was common with 73% of the cohort having 2 or more chronic conditions. (mean ± SD 2.75 ± 1.84, median = 2.00, range 0–13). The prevalence of multimorbidity increased with age, obesity, physical inactivity, tobacco smoking and family history of asthma, diabetes, myocardial infarct or cancer. There were 13 pairs and 27 triplets of conditions identified with a prevalence 1.5% and O/E 1.5. Of the triplets, arthritis ( 50%), bowel disease ( 33%) and depression-anxiety ( 33%) were observed most commonly. LCA modelling identified 4 statistically and clinically distinct classes of multimorbidity labelled as: 1) “Healthy” (70%) with average of 1.95 conditions 2) “Respiratory and Atopy” (11%, 3.65 conditions) 3) “Non-cardiometabolic” (14%, 4.77 conditions), and 4) “Cardiometabolic” (5%, 6.32 conditions). Predictors of multimorbidity class membership differed between classes and differed from predictors of number of co-occurring conditions. Multimorbidity is common among middle-aged adults from a general population. Some conditions associated with ageing such as arthritis, bowel disease and depression-anxiety co-occur in clinically distinct patterns and at higher prevalence than expected by chance. These findings may inform further studies into shared biological and environmental causes of co-occurring conditions of ageing. Recognition of distinct patterns of multimorbidity may aid in a holistic approach to care management in in iduals presenting with multiple chronic conditions, while also guiding health resource allocation in ageing populations.
Publisher: American Thoracic Society
Date: 07-2022
Publisher: Springer Science and Business Media LLC
Date: 26-05-2023
Publisher: Wiley
Date: 05-04-2021
DOI: 10.1002/PPUL.25386
Abstract: Long‐term childhood asthma studies that investigate adult outcomes other than respiratory morbidity are lacking. This study examines the associations of childhood asthma and the occurrence of cardiovascular disease (CVD) events and mortality in adulthood. A cohort of 4430 school children (aged 17 years) who attended the Busselton Health Study between 1967 and 1983 were analyzed. Self‐reported history of doctor‐diagnosed asthma was determined based on the questionnaire. Subsequent CVD events (hospital admissions or death) up to 2014 were identified using the Western Australia Data Linkage System. Cox regression models were used to investigate the impact of childhood asthma on CVD events and mortality in adulthood. A subgroup of 2153 participants who re‐attended a survey in young adulthood was also analyzed. A total of 462 (10%) of the cohort had childhood asthma. During follow‐up, 867 participants experienced a CVD event and 22 participants died from CVD. Childhood asthma was not associated with the risk of CVD events in adulthood (HR, 1.12 95% CI: 0.91–1.39 p = .2833) and this persisted after adjustment for confounders. Childhood asthma was not associated with coronary heart disease events (HR, 0.72 95% CI: 0.40–1.30 p = .2761), heart failure events (HR, 0.55 95% CI: 0.07–4.13 p = .5604) or CVD mortality (HR, 0.91 95% CI: 0.21–3.89 p = .8987) in adulthood. Childhood asthma is not associated with the risk of CVD events and mortality in adulthood.
Publisher: Wiley
Date: 09-03-2022
DOI: 10.1111/RESP.14240
Abstract: The airway smooth muscle (ASM) layer thickens during development. Identifying the mechanism(s) for normal structural maturation of the ASM reveals pathways susceptible to disease processes. This study characterized thickening of the ASM layer from foetal life to childhood and elucidated the underlying mechanism in terms of hypertrophy, hyperplasia and extracellular matrix (ECM) deposition. Airways from post‐mortem cases were examined from seven different age groups: 22–24 weeks gestation, 25–31 weeks gestation, term (37–41 weeks gestation), .5 year, 0.5–1 year, 2–5 years and 6–10 years. The ASM layer area (thickness), the number and size of ASM cells and the volume fraction of ECM were assessed by planimetry and stereology. From late gestation to the first year of life, normalized ASM thickness more than doubled as a result of ASM hypertrophy. Thereafter, until childhood, the ASM layer grew in proportion to airway size, which was mediated by ASM hyperplasia. Hypertrophy and hyperplasia of ASM were accompanied by a proportional change in ECM such that the broad composition of the ASM layer was constant across age groups. These data suggest that the mechanisms of ASM growth from late gestation to childhood are temporally decoupled, with early hypertrophy and subsequent proliferation. We speculate that the developing airway is highly susceptible to ASM thickening in the first year of life and that the timing of an adverse event will determine structural phenotype.
Publisher: American Thoracic Society
Date: 15-02-2023
Publisher: American Thoracic Society
Date: 08-2019
No related grants have been discovered for Alan James.