Adapting data collection methods in the Australian life histories and health survey: a retrospective life course study

OBJECTIVE Ideally, life course data are collected prospectively through an ongoing longitudinal study. We report adaptive multimethod fieldwork procedures that gathered life history data by mail survey and telephone interview, comparable with the face-to-face methods employed in the English Longitudinal Study on Ageing (ELSA). DESIGN The Australian Life Histories and Health (LHH) Survey was a substudy of the Australian 45 and Up Study, with data collection methods modified from the ELSA Study. A self-complete questionnaire and life history calendar were completed by the participants, followed by a computer-assisted telephone interview recording key life events. RESULTS The LHH survey developed and tested procedures and instruments that gathered rich life history data within an ongoing Australian longitudinal survey on ageing. Data collection proved to be economical. The use of a self-complete questionnaire in conjunction with a life history calendar and coordinated computer-assisted telephone interview was successful in collecting retrospective life course information, in terms of being thorough, practical and efficient. This study has a diverse collection of data covering the life course, starting with early life experiences and continuing with socioeconomic and health exposures and outcomes during adult life. CONCLUSIONS Mail and telephone methodology can accurately and economically add a life history dimension to an ongoing longitudinal survey. The method is particularly valuable for surveying widely dispersed populations. The results will facilitate understanding of the social determinants of health by gathering data on earlier life exposures as well as comparative data across geographical and societal contexts.Supported by an Australian Research Council Grant (DP 1096778, “Socio-economic determinants and health inequalities over the life-course: Australian and English comparisons”) with investigators from the Universities of Sydney, Newcastle and Queensland (Australia) and the University of Manchester (UK)

Aberrant Cytoplasm Localization and Protein Stability of SIRT1 is Regulated by PI3K/IGF-1R Signaling in Human Cancer Cells

SIRT1, an NAD-dependent histone/protein deacetylase, has classically been thought of as a nuclear protein. In this study, we demonstrate that SIRT1 is mainly localized in the nucleus of normal cells, but is predominantly localized in the cytoplasm of the cancer / transformed cells we tested. We found this predominant cytoplasmic localization of SIRT1 is regulated by elevated mitotic activity and PI3K/IGF-1R signaling in cancer cells. We show that aberrant cytoplasmic localization of SIRT1 is due to increased protein stability and is regulated by PI3K/IGF-1R signaling. In addition, we determined that SIRT1 is required for PI3K-mediated cancer cell growth. Our study represents the first identification that aberrant cytoplasm localization is one of the specific alternations to SIRT1 that occur in cancer cells, and PI3K/IGF-1R signaling plays an important role in the regulation of cytoplasmic SIRT1 stability. Our findings suggest that the over-expressed cytoplasmic SIRT1 in cancer cells may greatly contribute to its cancer-specific function by working downstream of the PI3K/IGF-1R signaling pathway

PI3Kγ is a molecular switch that controls immune suppression

Macrophages play critical, but opposite, roles in acute and chronic inflammation and cancer1,2,3,4,5. In response to pathogens or injury, inflammatory macrophages express cytokines that stimulate cytotoxic T cells, whereas macrophages in neoplastic and parasitic diseases express anti-inflammatory cytokines that induce immune suppression and may promote resistance to T cell checkpoint inhibitors1,2,3,4,5,6,7. Here we show that macrophage PI 3-kinase γ controls a critical switch between immune stimulation and suppression during inflammation and cancer. PI3Kγ signalling through Akt and mTor inhibits NFκB activation while stimulating C/EBPβ activation, thereby inducing a transcriptional program that promotes immune suppression during inflammation and tumour growth. By contrast, selective inactivation of macrophage PI3Kγ stimulates and prolongs NFκB activation and inhibits C/EBPβ activation, thus promoting an immunostimulatory transcriptional program that restores CD8+ T cell activation and cytotoxicity. PI3Kγ synergizes with checkpoint inhibitor therapy to promote tumour regression and increased survival in mouse models of cancer. In addition, PI3Kγ-directed, anti-inflammatory gene expression can predict survival probability in cancer patients. Our work thus demonstrates that therapeutic targeting of intracellular signalling pathways that regulate the switch between macrophage polarization states can control immune suppression in cancer and other disorders

More-than-Human Data Interactions in the Smart City - reflections

How might we design and plan urban spaces to be more hospitable for foxes? How might a worm or a nettle plant experience the neighbourhood we live in? What kinds of urban data might parakeets find useful? And how might we design new technologies for more equitable living spaces for all of London’s inhabitants - human and non-human, big and small? This booklet brings together reflections from a research project called “More-than- Human Data Interactions in the Smart City.” Through a series of probes and proposals, and two workshops in east London with participants that included community organisers, growers, policy-makers, activists, academics, educators and artists, we explored questions about who we share our city with, and how we can better live together with our non-human neighbours with the help of digital infrastructure and data

The future burden of lung cancer attributable to current modifiable behaviours: a pooled study of seven Australian cohorts

BACKGROUND: Knowledge of preventable disease and differences in disease burden can inform public health action to improve health and health equity. We quantified the future lung cancer burden preventable by behavioural modifications across Australia. METHODS: We pooled seven Australian cohort studies (n = 367 058) and linked them to national registries to identify lung cancers and deaths. We estimated population attributable fractions and their 95% confidence intervals (CIs) for modifiable risk factors, using risk estimates from the cohort data and risk factor exposure distribution from contemporary national health surveys. RESULTS: During the first 10-year follow-up, there were 2025 incident lung cancers and 20 349 deaths. Stopping current smoking could prevent 53.7% (95% CI, 50.0-57.2%) of lung cancers over 40 years and 18.3% (11.0-25.1%) in 10 years. The smoking-attributable burden is highest in males, those who smoke <20 cigarettes per day, are <75 years of age, unmarried, of lower educational attainment, live in remote areas or are healthy weight. Increasing physical activity and fruit consumption, if causal, could prevent 15.6% (6.9-23.4%) and 7.5% (1.3-13.3%) of the lung cancer burden, respectively. Jointly, the three behaviour modifications could prevent up to 63.0% (58.0-67.5%) of lung cancers in 40 years, and 31.2% (20.9-40.1%) or 43 300 cancers in 10 years. The preventable burden is highest among those with multiple risk factors. CONCLUSIONS: Smoking remains responsible for the highest burden of lung cancer in Australia. The uneven burden distribution distinguishes subgroups that could benefit the most from activities to control the world's deadliest cancer

More-than-human data interactions in the city

This booklet brings together reflections from a research project called “More-than- Human Data Interactions in the Smart City.” Through a series of probes and proposals, and two workshops in east London with participants that included community organisers, growers, policy-makers, activists, academics, educators and artists, we explored questions about who we share our city with, and how we can better live together with our non-human neighbours with the help of digital infrastructure and data

Standardization of surface electromyography utilized to evaluate patients with dysphagia

<p>Abstract</p> <p>Backgorund</p> <p>Patients suspected of having swallowing disorders, could highly benefit from simple diagnostic screening before being referred to specialist evaluations. We introduce surface electromyography (sEMG) to carry out rapid assessment of such patients and propose suggestions for standardizing sEMGs in order to identify abnormal deglutition.</p> <p>Methods</p> <p>Specifics steps for establishing standards for applying the technique for screening purposes (e.g., evaluation of specific muscles), the requirements for diagnostic sEMG equipment, the sEMG technique itself, and defining the tests suitable for assessing deglutition (e.g., saliva, normal, and excessive swallows and uninterrupted drinking of water) are presented in detail. A previously described normative database for single swallowing and drinking and standard approach to analysis was compared to data on the duration and electric activity of muscles involved in deglutition and with sEMG recordings in order to estimate stages of a swallow.</p> <p>Conclusion</p> <p>SEMG of swallowing is a simple and reliable method for screening and preliminary differentiation among dysphagia and odynophagia of various origins. This noninvasive radiation-free examination has a low level of discomfort, and is simple, timesaving and inexpensive to perform. With standardization of the technique and an established normative database, sEMG can serve as a reliable screening method for optimal patient management.</p

The burden of cancer attributable to modifiable risk factors: the Australian cancer-PAF cohort consortium

Purpose: To estimate the Australian cancer burden attributable to lifestyle-related risk factors and their combinations using a novel population attributable fraction (PAF) method that accounts for competing risk of death, risk factor interdependence and statistical uncertainty. Participants: 365 173 adults from seven Australian cohort studies. We linked pooled harmonised individual participant cohort data with population-based cancer and death registries to estimate exposure-cancer and exposure-death associations. Current Australian exposure prevalence was estimated from representative external sources. To illustrate the utility of the new PAF method, we calculated fractions of cancers causally related to body fatness or both tobacco and alcohol consumption avoidable in the next 10 years by risk factor modifications, comparing them with fractions produced by traditional PAF methods. Findings to date: Over 10 years of follow-up, we observed 27 483 incident cancers and 22 078 deaths. Of cancers related to body fatness (n=9258), 13% (95% CI 11% to 16%) could be avoided if those currently overweight or obese had body mass index of 18.5-24.9 kg/m2. Of cancers causally related to both tobacco and alcohol (n=4283), current or former smoking explains 13% (11% to 16%) and consuming more than two alcoholic drinks per day explains 6% (5% to 8%). The two factors combined explain 16% (13% to 19%): 26% (21% to 30%) in men and 8% (4% to 11%) in women. Corresponding estimates using the traditional PAF method were 20%, 31% and 10%. Our PAF estimates translate to 74 000 avoidable body fatness-related cancers and 40 000 avoidable tobacco- and alcohol-related cancers in Australia over the next 10 years (2017-2026). Traditional PAF methods not accounting for competing risk of death and interdependence of risk factors may overestimate PAFs and avoidable cancers. Future plans: We will rank the most important causal factors and their combinations for a spectrum of cancers and inform cancer control activities.Maria E Arriaga, Claire M Vajdic, Karen Canfell, Robert MacInnis, Peter Hull, Dianna J Magliano, Emily Banks, Graham G Giles, Robert G Cumming, Julie E Byles, Anne W Taylor, Jonathan E Shaw, Kay Price, Vasant Hirani, Paul Mitchell, Barbara-Ann Adelstein, Maarit A Laaksone