Background: Experimental and epidemiological studies indicate an association between exposure to particulate matter (PM) air pollution and increased risk of type 2 diabetes. In view of the high and increasing prevalen...
Background: Experimental and epidemiological studies indicate an association between exposure to particulate matter (PM) air pollution and increased risk of type 2 diabetes. In view of the high and increasing prevalence of diabetes, we aimed to quantify the burden of type 2 diabetes attributable to PM2·5 originating from ambient and household air pollution. Methods: We systematically compiled all relevant cohort and case-control studies assessing the effect of exposure to household and ambient fine particulate matter (PM2·5) air pollution on type 2 diabetes incidence and mortality. We derived an exposure–response curve from the extracted relative risk estimates using the MR-BRT (meta-regression—Bayesian, regularised, trimmed) tool. The estimated curve was linked to ambient and household PM2·5 exposures from the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, and estimates of the attributable burden (population attributable fractions and rates per 100 000 population of deaths and disability-adjusted life-years) for 204 countries from 1990 to 2019 were calculated. We also assessed the role of changes in exposure, population size, age, and type 2 diabetes incidence in the observed trend in PM2·5-attributable type 2 diabetes burden. All estimates are presented with 95% uncertainty intervals. Findings: In 2019, approximately a fifth of the global burden of type 2 diabetes was attributable to PM2·5 exposure, with an estimated 3·78 (95% uncertainty interval 2·68–4·83) deaths per 100 000 population and 167 (117–223) disability-adjusted life-years (DALYs) per 100 000 population. Approximately 13·4% (9·49–17·5) of deaths and 13·6% (9·73–17·9) of DALYs due to type 2 diabetes were contributed by ambient PM2·5, and 6·50% (4·22–9·53) of deaths and 5·92% (3·81–8·64) of DALYs by household air pollution. High burdens, in terms of numbers as well as rates, were estimated in Asia, sub-Saharan Africa, and South Am
Brain-machine interface (BMI) performance has been improved using Kalman filters (KF) combined with closed-loop decoder adaptation (CLDA). CLDA fits the decoder parameters during closed-loop BMI operation based on the...
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Brain-machine interface (BMI) performance has been improved using Kalman filters (KF) combined with closed-loop decoder adaptation (CLDA). CLDA fits the decoder parameters during closed-loop BMI operation based on the neural activity and inferred user velocity intention. These advances have resulted in the recent ReFIT-KF and SmoothBatch-KF decoders. Here we demonstrate high-performance and robust BMI control using a novel closed-loop BMI architecture termed adaptive optimal feedback-controlled (OFC) point process filter (PPF). Adaptive OFC-PPF allows subjects to issue neural commands and receive feedback with every spike event and hence at a faster rate than the KF. Moreover, it adapts the decoder parameters with every spike event in contrast to current CLDA techniques that do so on the time-scale of minutes. Finally, unlike current methods that rotate the decoded velocity vector, adaptive OFC-PPF constructs an infinite-horizon OFC model of the brain to infer velocity intention during adaptation. Preliminary data collected in a monkey suggests that adaptive OFC-PPF improves BMI control. OFC-PPF outperformed SmoothBatch-KF in a self-paced center-out movement task with 8 targets. This improvement was due to both the PPF's increased rate of control and feedback compared with the KF, and to the OFC model suggesting that the OFC better approximates the user's strategy. Also, the spike-by-spike adaptation resulted in faster performance convergence compared to current techniques. Thus adaptive OFC-PPF enabled proficient BMI control in this monkey.
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