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1.
  • Bixby, H., et al. (författare)
  • Rising rural body-mass index is the main driver of the global obesity epidemic in adults
  • 2019
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 569:7755, s. 260-4
  • Tidskriftsartikel (refereegranskat)abstract
    • Body-mass index (BMI) has increased steadily in most countries in parallel with a rise in the proportion of the population who live in cities(.)(1,2) This has led to a widely reported view that urbanization is one of the most important drivers of the global rise in obesity(3-6). Here we use 2,009 population-based studies, with measurements of height and weight in more than 112 million adults, to report national, regional and global trends in mean BMI segregated by place of residence (a rural or urban area) from 1985 to 2017. We show that, contrary to the dominant paradigm, more than 55% of the global rise in mean BMI from 1985 to 2017-and more than 80% in some low- and middle-income regions-was due to increases in BMI in rural areas. This large contribution stems from the fact that, with the exception of women in sub-Saharan Africa, BMI is increasing at the same rate or faster in rural areas than in cities in low- and middle-income regions. These trends have in turn resulted in a closing-and in some countries reversal-of the gap in BMI between urban and rural areas in low- and middle-income countries, especially for women. In high-income and industrialized countries, we noted a persistently higher rural BMI, especially for women. There is an urgent need for an integrated approach to rural nutrition that enhances financial and physical access to healthy foods, to avoid replacing the rural undernutrition disadvantage in poor countries with a more general malnutrition disadvantage that entails excessive consumption of low-quality calories.
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2.
  • Liu, Y., et al. (författare)
  • Anthropogenic Aerosols Cause Recent Pronounced Weakening of Asian Summer Monsoon Relative to Last Four Centuries
  • 2019
  • Ingår i: Geophysical Research Letters. - : American Geophysical Union (AGU). - 0094-8276 .- 1944-8007. ; 46:10, s. 5469-5479
  • Tidskriftsartikel (refereegranskat)abstract
    • The Asian Summer Monsoon (ASM) affects ecosystems, biodiversity, and food security of billions of people. In recent decades, ASM strength (as represented by precipitation) has been decreasing, but instrumental measurements span only a short period of time. The initiation and the dynamics of the recent trend are unclear. Here for the first time, we use an ensemble of 10 tree ring-width chronologies from the west-central margin of ASM to reconstruct detail of ASM variability back to 1566 CE. The reconstruction captures weak/strong ASM events and also reflects major locust plagues. Notably, we found an unprecedented 80-year trend of decreasing ASM strength within the context of the 448-year reconstruction, which is contrary to what is expected from greenhouse warming. Our coupled climate model shows that increasing anthropogenic sulfate aerosol emissions over the Northern Hemisphere could be the dominant factor contributing to the ASM decrease. Plan Language Summary Monsoonal rainfall has a certain influence on agriculture and industry in the regions of Asian Summer Monsoon (ASM). An understanding of the spatial-temporal variability of the ASM and the associated dynamics is vital for terrestrial ecosystems, water resources, forests, and landscapes. We have developed a 448-year ASM reconstruction back to 1566 CE using 10 tree ring chronologies from the margin region of ASM. We find that historical severe droughts and locust plague disasters during weak ASM events. The recent decreasing ASM trend persisting for over 80 years is unprecedented over the past 448 years. Coupled climate models show that increasing anthropogenic aerosol emissions are the dominant underlying factor. Our aim is that the time series will find a wide range of utility for understanding past climate variability and for predicting future climate change.
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  • Ruilope, LM, et al. (författare)
  • Design and Baseline Characteristics of the Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease Trial
  • 2019
  • Ingår i: American journal of nephrology. - : S. Karger AG. - 1421-9670 .- 0250-8095. ; 50:5, s. 345-356
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Background:</i></b> Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. <b><i>Patients and</i></b> <b><i>Methods:</i></b> The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate ≥25 mL/min/1.73 m<sup>2</sup> and albuminuria (urinary albumin-to-creatinine ratio ≥30 to ≤5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level α = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. <b><i>Conclusions:</i></b> FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049.
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