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- Mishra, A, et al.
(author)
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Diminishing benefits of urban living for children and adolescents' growth and development
- 2023
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In: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 615:7954, s. 874-883
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Journal article (peer-reviewed)abstract
- Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified.
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- Taddei, C, et al.
(author)
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Repositioning of the global epicentre of non-optimal cholesterol
- 2020
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In: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 582:7810, s. 73-
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Journal article (peer-reviewed)abstract
- High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol—which is a marker of cardiovascular risk—changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million–4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world.
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- Guo, J, et al.
(author)
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Body Mass Index Trajectories Preceding Incident Mild Cognitive Impairment and Dementia
- 2022
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In: JAMA psychiatry. - : American Medical Association (AMA). - 2168-6238 .- 2168-622X. ; 79:12, s. 1180-1187
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Journal article (peer-reviewed)abstract
- Body mass index (BMI) trajectories before the onset of mild cognitive impairment (MCI) and during the progression from MCI to dementia remain unclear.ObjectiveTo assess the long-term BMI trajectories preceding incident MCI and dementia and explore whether they are associated with brain pathologies.Design, Setting, and ParticipantsThe Rush Memory and Aging Project (MAP) was an ongoing community-based cohort study. This study included cognitively intact participants aged 60 to 90 years at baseline with annual follow-up from October 1997 to December 2020 (maximum follow-up of 22 years). During the follow-up, participants underwent brain autopsies. Data were analyzed from August 2021 to February 2022 using mixed-effect models.ExposuresBMI was calculated using height and weight measured at baseline and follow-ups.Main Outcomes and MeasuresIncident MCI and dementia were diagnosed following standard criteria. Neuropathological assessments (including global Alzheimer disease and vascular pathology) were performed for autopsies.ResultsA total of 1390 participants (mean [SD] age, 78.4 [6.5] years; 1063 female [76.5%]) were included in the study. In the analysis of BMI trajectories before MCI (n = 939), during the follow-up (median [IQR] duration, 6 [3-9] years), 371 participants (39.5%) developed MCI, of whom 88 (23.7%) progressed to dementia. Those who developed MCI were older (mean [SD] age, 79.6 [5.9] years vs 76.9 [6.6] years), consumed less alcohol (median [IQR] consumption, 0 [0-5.8] g/day vs 1.1 [0-6.9] g/day), had a lower BMI (mean [SD], 27.2 [4.9] vs 28.2 [5.9]), and were more likely to be apolipoprotein E (APOE) ε4 carriers (89 of 371 [24.0%] vs 98 of 568 [17.3%]) compared with those who remained cognitively intact over follow-up. Those who developed dementia were older (mean [SD] age, 81.0 [5.2] years vs 79.1 [6.0] years), had a lower level of physical activity (median [IQR] activity, 1.0 [0-2.5] h/week vs 1.8 [0.2-3.8] h/week), and were more likely to be APOE ε4 carriers than those who were dementia-free (33 of 88 [37.5%] vs 56 of 283 [19.8%]). Compared with participants who remained cognitively intact, in those with incident MCI, BMI tended to decline earlier and faster. From 7 years before diagnosis, people with incident MCI had an associated significantly lower BMI (mean difference, −0.96; 95% CI, −1.85 to −0.07) than those who were cognitively intact. Among people with incident MCI, the slopes of BMI decline did not differ significantly between those who did and did not develop dementia (β, −0.03; 95% CI, −0.21 to 0.15). In the analysis of BMI trajectories before autopsy (n = 358), BMI was associated with a faster declination among participants with a high burden of global Alzheimer disease pathology (β for pathology × time highest vs lowest tertile, −0.14; 95% CI, −0.26 to −0.02) or vascular pathology (β for pathology × time2 highest vs lowest tertile, 0.02; 95% CI, 0-0.05).Conclusions and RelevanceResults of this cohort study suggest that among cognitively intact people, significantly lower BMI occurs beginning approximately 7 years before MCI diagnosis. After MCI diagnosis, BMI declines at the same pace in people who develop dementia and those who do not. High brain pathologies may underly the BMI decline preceding dementing disorders.
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- Kvedaraite, E, et al.
(author)
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Notch-dependent cooperativity between myeloid lineages promotes Langerhans cell histiocytosis pathology
- 2022
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In: Science immunology. - : American Association for the Advancement of Science (AAAS). - 2470-9468. ; 7:78, s. eadd3330-
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Journal article (peer-reviewed)abstract
- Langerhans cell histiocytosis (LCH) is a potentially fatal neoplasm characterized by the aberrant differentiation of mononuclear phagocytes, driven by mitogen-activated protein kinase (MAPK) pathway activation. LCH cells may trigger destructive pathology yet remain in a precarious state finely balanced between apoptosis and survival, supported by a unique inflammatory milieu. The interactions that maintain this state are not well known and may offer targets for intervention. Here, we used single-cell RNA-seq and protein analysis to dissect LCH lesions, assessing LCH cell heterogeneity and comparing LCH cells with normal mononuclear phagocytes within lesions. We found LCH discriminatory signatures pointing to senescence and escape from tumor immune surveillance. We also uncovered two major lineages of LCH with DC2- and DC3/monocyte-like phenotypes and validated them in multiple pathological tissue sites by high-content imaging. Receptor-ligand analyses and lineage tracing in vitro revealed Notch-dependent cooperativity between DC2 and DC3/monocyte lineages during expression of the pathognomonic LCH program. Our results present a convergent dual origin model of LCH with MAPK pathway activation occurring before fate commitment to DC2 and DC3/monocyte lineages and Notch-dependent cooperativity between lineages driving the development of LCH cells.
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