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  • 1
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 106, No. 12 ( 2011-12-28), p. 1899-1914
    Abstract: The National Diet and Nutrition Survey (NDNS) is a cross-sectional survey designed to gather data representative of the UK population on food consumption, nutrient intakes and nutritional status. The objectives of the present paper were to identify and describe food consumption and nutrient intakes in the UK from the first year of the NDNS rolling programme (2008–09) and compare these with the 2000–01 NDNS of adults aged 19–64 years and the 1997 NDNS of young people aged 4–18 years. Differences in median daily food consumption and nutrient intakes between the surveys were compared by sex and age group (4–10 years, 11–18 years and 19–64 years). There were no changes in energy, total fat or carbohydrate intakes between the surveys. Children aged 4–10 years had significantly lower consumption of soft drinks (not low calorie), crisps and savoury snacks and chocolate confectionery in 2008–09 than in 1997 (all P   〈  0·0001). The percentage contribution of non-milk extrinsic sugars to food energy was also significantly lower than in 1997 in children aged 4–10 years ( P   〈  0·0001), contributing 13·7–14·6 % in 2008–09 compared with 16·8 % in 1997. These changes were not as marked in older children and there were no changes in these foods and nutrients in adults. There was still a substantial proportion (46 %) of girls aged 11–18 years and women aged 19–64 years (21 %) with mean daily Fe intakes below the lower reference nutrient intake. Since previous surveys there have been some positive changes in intakes especially in younger children. However, further attention is required in other groups, in particular adolescent girls.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2011
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    SSG: 21
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  • 2
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 107, No. 3 ( 2012-02-14), p. 405-415
    Abstract: High saturated fat intake is an established risk factor for several chronic diseases. The objective of the present study is to report dietary intakes and main food sources of fat and fatty acids (FA) from the first year of the National Diet and Nutrition Survey (NDNS) rolling programme in the UK. Dietary data were collected using 4 d estimated food diaries ( n 896) and compared with dietary reference values (DRV) and previous NDNS results. Total fat provided 34–36 % food energy (FE) across all age groups, which was similar to previous surveys for adults. Men (19–64 years) and older girls (11–18 years) had mean intakes just above the DRV, while all other groups had mean total fat intakes of 〈  35 % FE. SFA intakes were lower compared with previous surveys, ranging from 13 to 15 % FE, but still above the DRV. Mean MUFA intakes were 12·5 % FE for adults and children aged 4–18 years and all were below the DRV. Mean n -3 PUFA intake represented 0·7–1·1 % FE. Compared with previous survey data, the direction of change for n -3 PUFA was upwards for all age groups, although the differences in absolute terms were very small. Trans -FA intakes were lower than in previous NDNS and were less than 2 g/d for all age groups, representing 0·8 % FE and lower than the DRV in all age groups. In conclusion, dietary intake of fat and FA is moving towards recommended levels for the UK population. However, there remains room for considerable further improvement.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2012
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    SSG: 12
    SSG: 21
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  • 3
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 2010
    In:  British Journal of Nutrition Vol. 103, No. 10 ( 2010-05-28), p. 1398-1403
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 103, No. 10 ( 2010-05-28), p. 1398-1403
    Abstract: Previous cell culture-based studies have shown potential health beneficial effects on gene expression of dietary polyphenols, including those found in red wine and green tea. However, these studies have tended to use higher concentrations (2–100 μ m ) than those observed in blood (0·1–1 μ m ) after consuming polyphenol-rich foods or beverages. The present study investigated effects of physiological concentrations of different classes of dietary polyphenol on the expression of genes important in cardiovascular health (endothelial NO synthase (eNOS), endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF)) by cultured vascular endothelial cells (human umbilical vein endothelial cells) in the absence or presence of H 2 O 2 . Resveratrol and quercetin (0·1–1 μ m ) increased eNOS and VEGF mRNA expression particularly in the absence of H 2 O 2 (50 μ m ) and decreased H 2 O 2 -induced ET-1 mRNA expression ( P   〈  0·001 for polyphenol × H 2 O 2 interactions). Similarly, resveratrol and quercetin decreased endothelin secretion into the media, blocking the stimulatory effect of 50 μ m -H 2 O 2 ( P   〈  0·001 for polyphenol × H 2 O 2 interaction). Of the nine other polyphenols tested, only epigallocatechin gallate had similar effects on both the eNOS and ET-1 mRNA expression, but to a lesser extent than resveratrol at an equimolar concentration (0·1 μ m ). The observed effects on gene expression would be expected to result in vasodilation and thereby reduced blood pressure. Since only three of the eleven polyphenols tested had biological activity, it is unclear whether particular structures are important or whether the effects might relate to the relatively high antioxidant capacities of the three active polyphenols.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2010
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
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  • 4
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 2008
    In:  Proceedings of the Nutrition Society Vol. 67, No. 1 ( 2008-02), p. 42-47
    In: Proceedings of the Nutrition Society, Cambridge University Press (CUP), Vol. 67, No. 1 ( 2008-02), p. 42-47
    Abstract: Previous studies have shown that consumption of fruit and vegetables plays a role in preventing the onset of CVD. These beneficial effects have been linked to the presence of polyphenolic compounds in plant-derived foods and their antioxidant capacity. It has been hypothesised that polyphenols may also have a direct effect on vascular endothelial cell growth and the expression of genes involved in angiogenesis and other roles of the endothelium. Previous studies in this area have tended to use concentrations of polyphenols that are supraphysiological (1–100 μ m ). The effects of more physiological concentrations (0·1 μ m ) of various individual polyphenols on gene expression were therefore investigated in cultured human umbilical vein endothelial cells (HUVEC) using both microarray and quantitative RT–PCR methodologies. Treatment of HUVEC with ferulic acid, quercetin or resveratrol (0·1 μ m ) resulted in changes to gene expression that for the three treatments amounted to significant ( 〉 2-fold) down-regulation of the expression of 363 genes and significant ( 〉 2-fold) up-regulation of 233 genes of the 10 000 genes present on the microarray. The majority of these genes were affected by resveratrol. Quantitative RT–PCR studies indicated that resveratrol (0·1 μ m ) significantly increased the expression of the gene encoding endothelial NO synthase (eNOS), which synthesises the vasodilator molecule NO, and both resveratrol and quercetin decreased expression of the potent vasoconstrictor, endothelin-1 (ET-1), while ferulic acid had no effect. The effects of resveratrol (0·1 μ m ) were also investigated when HUVEC were under oxidative stress following treatment with H 2 O 2 (0–50 μ m ), which dose-dependently increased expression of eNOS and ET-1. Resveratrol stimulated eNOS mRNA in the absence of H 2 O 2 and still allowed the increase with H 2 O 2 , but the effects were not additive. In contrast, resveratrol blocked the stimulatory effect of H 2 O 2 on ET-1 expression. Hence, resveratrol has potent effects at a physiological concentration (0·1 μ m ) that would be expected to result in vasodilation and therefore help reduce blood pressure and the risk of CVD.
    Type of Medium: Online Resource
    ISSN: 0029-6651 , 1475-2719
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2008
    detail.hit.zdb_id: 2016335-6
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  • 5
    Online Resource
    Online Resource
    Informa UK Limited ; 2004
    In:  Biocatalysis and Biotransformation Vol. 22, No. 5-6 ( 2004-12), p. 397-400
    In: Biocatalysis and Biotransformation, Informa UK Limited, Vol. 22, No. 5-6 ( 2004-12), p. 397-400
    Type of Medium: Online Resource
    ISSN: 1024-2422 , 1029-2446
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2004
    detail.hit.zdb_id: 2043266-5
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  • 6
    In: Nature, Springer Science and Business Media LLC, Vol. 600, No. 7889 ( 2021-12-16), p. 472-477
    Abstract: The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-19 1,2 , host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases 3–7 . They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
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  • 7
    In: Nature, Springer Science and Business Media LLC, Vol. 621, No. 7977 ( 2023-09-07), p. E7-E26
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
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  • 8
    In: Nature, Springer Science and Business Media LLC, Vol. 617, No. 7962 ( 2023-05-25), p. 764-768
    Abstract: Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown 1 to be highly efficient for discovery of genetic associations 2 . Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group 3 . Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling ( JAK1 ), monocyte–macrophage activation and endothelial permeability ( PDE4A ), immunometabolism ( SLC2A5 and AK5 ), and host factors required for viral entry and replication ( TMPRSS2 and RAB2A ).
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
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  • 9
    In: Nature, Springer Science and Business Media LLC, Vol. 619, No. 7971 ( 2023-07-27), p. E61-E61
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
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  • 10
    In: Nature, Springer Science and Business Media LLC, Vol. 607, No. 7917 ( 2022-07-07), p. 97-103
    Abstract: Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care 1 or hospitalization 2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling ( IL10RB and PLSCR1 ), leucocyte differentiation ( BCL11A ) and blood-type antigen secretor status ( FUT2 ). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase ( ATP11A ), and increased expression of a mucin ( MUC1 )—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules ( SELE , ICAM5 and CD209 ) and the coagulation factor F8 , all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease.
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
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