546 research outputs found

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    Rufus Jones and Mysticism

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    Using botanic gardens and arboreta to help identify urban trees for the future

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    Societal Impact StatementDiversification of urban forests is essential to enhance their resilience to future biotic threats as well as those posed by a changing climate. Arboreta and botanic gardens host a wide range of plant material that can be evaluated to inform tree selection policy. This study demonstrates that plant functional traits, such as the water potential at leaf turgor loss, can be highly instructive when developing evidence-based recommendations for urban environments. However, if botanic collections are to fulfil a critical role in understanding plant response to environment, they should not be managed solely as visitor attractions but must have scientific objectives at the forefront of management policy.SummaryArboreta and botanic gardens host a multitude of species that can be utilized in research focused on improving diversity within urban forests. Higher tree species diversity will enhance the resilience of urban forests to abiotic and biotic threats and help deliver strategies that foster sustainable communities. Consequently, this study aims to demonstrate the value of botanic collections as a resource for research into tree species selection for more resilient urban landscapes. As water stress is a major constraint for trees in urban environments, understanding the drought tolerance of species is essential for urban tree selection. This study evaluates a key functional trait relating to drought tolerance. Using vapor pressure osmometry, the water potential at leaf turgor loss was evaluated for 96 species using plant material from seven botanic collections in North America and Europe. Leaf turgor loss contrasted widely in the temperate deciduous trees evaluated and, in summer, ranged from -1.7 MPa to -3.9 MPa. Significant differences in drought tolerance were also apparent across genera and closely related cultivars. Osmotic adjustment was shown to be a major physiological factor driving leaf turgor loss. A meta-analysis also demonstrated that leaf turgor loss was closely related to a drought-tolerance scale based on observations of tree performance under drought. Arboreta and botanic collections can play a vital role in the evaluation of plant material for urban environments, provided they are curated with scientific objectives at the forefront of management policy and are not managed purely as visitor attractions

    Socioeconomic Inequalities in Mortality Rates in Old Age in the World Health Organization Europe Region

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    Socioeconomic adversity is among the foremost fundamental causes of human suffering, and this is no less true in old age. Recent reports on socioeconomic inequalities in mortality rate in old age suggest that a low socioeconomic position continues to increase the risk of death even among the oldest old. We aimed to examine the evidence for socioeconomic mortality rate inequalities in old age, including information about associations with various indicators of socioeconomic position and for various geographic locations within the World Health Organization Region for Europe. The articles included in this review leave no doubt that inequalities in mortality rate by socioeconomic position persist into the oldest ages for both men and women in all countries for which information is available, although the relative risk measures observed were rarely higher than 2.00. Still, the available evidence base is heavily biased geographically, inasmuch as it is based largely on national studies from Nordic and Western European countries and local studies from urban areas in Southern Europe. This bias will hamper the design of European-wide policies to reduce inequalities in mortality rate. We call for a continuous update of the empiric evidence on socioeconomic inequalities in mortality rate

    SPARC is expressed in renal interstitial fibrosis and in renal vascular injury

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    SPARC is expressed in renal interstitial fibrosis and in renal vascular injury. Tubulointerstitial inflammation and fibrosis are critical determinants for renal function and prognosis in a variety of human nephropathies. Yet, the pathophysiology of the injury remains obscure. We investigated the expression of SPARC (secreted protein acidic and rich in cysteine) by immunohistochemistry and in situ hybridization in experimental models characterized by tubulointerstitial fibrosis and matrix expansion in rats. SPARC is a secreted glycoprotein that has been demonstrated to affect cellular interaction with matrix proteins, modulate cell proliferation, bind to and/or inhibit growth factors such as PDGF and bFGF, and regulate angiogenesis. Interstitial expression of SPARC was most prominent in passive Heyman nephritis (PHN), chronic cyclosporine A (CsA) nephropathy, and the remnant kidney model and, to a lesser extent, in angiotensin II (Ang II)-infused animals. SPARC protein and mRNA were substantially increased at sites of tubulointerstitial fibrosis/matrix expansion. In the PHN model, SPARC protein was expressed by interstitial fibroblasts that also produced α-smooth muscle actin (“myofibroblasts”) and correlated both temporally (r = 0.97) and spatially with sites of type I collagen deposition. Interstitial cell proliferation preceded the development of interstitial fibrosis, and maximal SPARC expression (d15) coincided with the initial decline in interstitial proliferation. In the Ang II-infusion model, which is characterized by arteriolopathy and tubulointerstitial injury, an increase in SPARC protein and mRNA was also seen in injured blood vessels. SPARC was shown to be expressed by vascular smooth muscle cells and also by cells in the adventitia of hypertrophied arteries. In summary, SPARC was transiently expressed by interstitial fibroblasts at sites of tubulointerstitial injury and fibrosis, and by smooth muscle cells and cells in the adventitia of injured arteries in the Ang II-model. In addition to its proposed role in extracellular matrix deposition, the antiproliferative properties of SPARC might contribute to the resolution of interstitial fibroblast proliferation in the PHN model

    Extracellular superoxide dismutase (SOD3) regulates oxidative stress at the vitreoretinal interface

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    Oxidative stress is a pathogenic feature in vitreoretinal disease. However, the ability of the inner retina to manage metabolic waste and oxidative stress is unknown. Proteomic analysis of antioxidants in the human vitreous, the extracellular matrix opposing the inner retina, identified superoxide dismutase-3 (SOD3) that localized to a unique matrix structure in the vitreous base and cortex. To determine the role of SOD3, Sod3-/- mice underwent histological and clinical phenotyping. Although the eyes were structurally normal, at the vitreoretinal interface Sod3-/- mice demonstrated higher levels of 3-nitrotyrosine, a key marker of oxidative stress. Pattern electroretinography also showed physiological signaling abnormalities within the inner retina. Vitreous biopsies and epiretinal membranes collected from patients with diabetic vitreoretinopathy (DVR) and a mouse model of DVR showed significantly higher levels of nitrates and/or 3-nitrotyrosine oxidative stress biomarkers suggestive of SOD3 dysfunction. This study analyzes the molecular pathways that regulate oxidative stress in human vitreous substructures. The absence or dysregulation of the SOD3 antioxidant at the vitreous base and cortex results in increased oxidative stress and tissue damage to the inner retina, which may underlie DVR pathogenesis and other vitreoretinal diseases

    Activity loss is associated with cognitive decline in age-related macular degeneration.

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    BACKGROUND/METHODS: The objective of this study was to determine whether relinquishing cognitive, physical, and social activities is associated with an increased risk of cognitive decline in patients with age-related macular degeneration (AMD). We conducted a 3-year longitudinal study of 206 nondemented patients with AMD. RESULTS: Twenty-three subjects (14.4%) declined cognitively. Age, sex, education, decline in visual acuity, and number of dropped activities were associated with cognitive decline; each additional dropped activity increased the risk by 58%. Subjects who relinquished three activities were 3.87 times (95% confidence interval, 1.95-7.76) more likely to become demented than subjects who relinquished no activities; those who relinquished five activities were 9.54 times (95% confidence interval, 3.05-30.43) more likely. A multivariate model demonstrated that number of dropped activities was a powerful predictor of cognitive decline after controlling for relevant risk factors, particularly for subjects younger than 80 years of age. CONCLUSIONS: Relinquishing valued activities is associated with an increased risk of cognitive decline in older patients with vision loss caused by AMD. These data suggest the importance of promoting optimal cognitive and physical health in patients with AMD and perhaps other chronic diseases

    Social isolation in childhood and adult inflammation: Evidence from the National Child Development Study

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    Background: Social isolation is known to be associated with poorer health amongst adults, including coronary heart disease. It is hypothesized that this association may be mediated by inflammation. There has been little prospective research on the long-term impact of social isolation in childhood on adult health or the pathways which might be involved. The aim of this study was to investigate whether social isolation in childhood is associated with increased adult inflammation and the mechanisms involved across the life course. Methods: This study used multiply-imputed data on 7462 participants of the National Child Development Study in Great Britain. The association between child social isolation (7-11. yrs) and levels of C-reactive protein (CRP) in middle age (44. yrs) was examined. We additionally investigated the role of adult social isolation, psychological distress, health behaviors and socioeconomic factors as potential mediators using path analysis and concurrent measurements made across the life course. Results: Socially isolated children had higher levels of C-reactive protein in mid-life (standardized coefficient. =. 0.05, p≤. 0.001). In addition, children who were socially isolated tended to have lower subsequent educational attainment, be in a less advantaged social class in adulthood, were more likely to be psychologically distressed across adulthood and were more likely to be obese and to smoke. All of these factors partially explained the association between childhood social isolation and CRP. However, this association remained statistically significant after considering all mediators simultaneously. Conclusions: Social isolation in childhood is associated with higher levels of C-reactive protein in mid-life. This is explained in part through complex mechanisms acting across the life course. Identification and interventions targeted toward socially isolated children may help reduce long-term adult health risk
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