308 research outputs found
APOE genotype and entorhinal cortex volume in non-demented community-dwelling adults in midlife and early old age
Copyright © 2012 IOS PressThis article has been made available through the Brunel Open Access Publishing Fund.The apolipoprotein E (APOE) ε4 allele is a risk factor for the neuropathological decline accompanying Alzheimer's disease (AD) while, conversely, the ε2 allele offers protection. One of the brain structures exhibiting the earliest changes associated with the disease is the entorhinal cortex. We therefore investigated the volumes of the entorhinal cortex and other structures in the medial temporal lobe including the parahippocampal gyrus, temporal pole, and inferior, middle, and superior temporal cortices, in relation to APOE genotype. Our main objectives were to determine if (a) volumes systematically varied according to allele in a stepwise fashion, ε2 > ε3 > ε4, and (b) associations varied according to age. We investigate this association in 627 non-demented community-dwelling adults in middle age (44 to 48 years; n = 314) and older age (64 to 68 years; n = 313) who underwent structural MRI scans. We found no evidence of APOE-related variation in brain volumes in the age groups examined. We conclude that if a ε2 > ε3 > ε4 pattern in brain volumes does emerge in non-demented adults living in the community in old age, it is not until after the age of 68 years.This study was funded by the UK Leverhulme
Trust, the British Academy, the NHMRC
Research Fellowship No. 471501, the NHMRC Research Fellowship No.#1002560, the National Health and Medical Research Council of Australia Unit Grant No. 973302, Program Grant No. 179805, Project grant No. 157125; Program grant no. 350833, and the National Computational Infrastructure. This article is made available through the Brunel Open Access Publishing Fund
Beyond platitudes: a qualitative study of Australian Aboriginal people's perspectives on biobanking.
BACKGROUND: Biobanks are vital resources for genetics and genomics, and it is broadly recognised that for maximal benefit it is essential that they include samples and data from diverse ancestral groups. The inclusion of First Nations people, in particular, is important to prevent biobanking research from exacerbating existing health inequities, and to ensure that these communities share in the benefits arising from research. AIMS: To explore the perspectives of Australian Aboriginal people whose tissue - or that of their family members - has been stored in the biobank of the National Centre for Indigenous Genomics (NCIG). METHODS: Semi-structured interviews with 42 Aboriginal people from the Titjikala, Galiwinku, Tiwi Islands, Yarrabah, Fitzroy Crossing, Derby, One Arm Point and Mulan communities, as well as a formal discussion with A. Hermes, an Indigenous Community Engagement Coordinator at the NCIG who had conducted the interviews. The interviews and the structured discussion were double coded using a procedure informed by Charmaz's outline of grounded theory analysis and Morse's outline of the cognitive basis of qualitative research. RESULTS: In this article, we report on A. Hermes' interviews with members from the above Aboriginal communities, as well as on her personal views, experiences, and interpretations of the interviews she conducted with other community members. We found that participation in the NCIG biobank raised issues around broken trust, grief and loss, but also - somewhat unexpectedly - was perceived as a source of empowerment, hope and reconnection. CONCLUSIONS: This research reminds us (again) of the need to engage deeply with communities in order to respond appropriately with respect for their cultural values and norms, and to develop culturally relevant policies and processes that enhance the benefits of biobank participation and minimise potential harms
Reducing domestic food waste by lowering home refrigerator temperatures
Domestic refrigerators often operate at temperatures which are higher than ideal for chilled food storage, with several studies finding averages around 7 C. Reducing temperatures for example to 4 C could significantly extend storage lives, giving greater opportunity for use before disposal. However, the savings in costs and emissions associated with reduced waste must be balanced against those associated with increased energy consumption at lower temperatures. Based on published storage lives of foods which are currently refrigerated and UK waste statistics, reducing from 7 C to 4 C could save £162.9 m of waste annually, with associated emissions of 270,000 tonnes CO2e. Including certain foods which are not always refrigerated and removing others which do not benefit from refrigeration, the estimated savings increased to £283.8 m and 578,383 tonnes CO2e. Based on experimental assessment, the costs and emissions associated with increased fridge energy consumption were considerably lower at £80.9 m and 367,411 tonnes CO2e. © 2013 Elsevier Ltd and IIR. All rights reserved
The potential for saving food waste by lowering home refrigerator temperatures
A significant proportion of the 4.4 million tonnes of avoidable household food and drink thrown away each year in the UK comprises products that require, or benefit from, refrigerated storage e.g. meat and fish, dairy products, most fruit and vegetables. In some consumers’ homes, refrigerated foods are kept in less than optimal conditions e.g. not in the refrigerator, ‘unwrapped’ or at refrigerator temperatures above 5oC. This can lead to rapid food spoilage, and also to food safety risks. Storage in the refrigerator at temperatures below 5oC could extend the storage life of many of these foods, giving greater opportunity for their consumption before they reach the end of their acceptable life. This paper presents results from research funded by WRAP to determine relationships between chilled storage temperature and published storage lives of typical food products. The potential reductions in food waste which might result from extended storage lives if refrigerator temperatures were lowered to 4°C rather than the UK average of 7°C (WRAP, 2010) are estimated. To be balanced against these savings however is the increased energy consumption which results from running refrigerators at lower temperatures, and results from an experimental assessment of the impact of lowering fridge temperatures on energy consumption are presented. The costs and associated carbon dioxide equivalent (CO2e) emissions associated with the saved waste and the increased energy are compared
Reducing domestic food waste by freezing at home
It is estimated that over 630,000 tonnes of 'freezable' food, worth up to £2.3 billion, are thrown away by UK consumers each year due to having passed labelled 'use by' dates or being perceived to have spoilt. Much of this food could instead have been frozen for later consumption, but research has shown that consumers are often uncertain about suitability of products for home freezing. A two-part study was therefore undertaken, starting with a literature and internet-based information review which found that although the majority of products are reported as suitable for home freezing, there is conflicting advice on some products and also marked differences between reported storage lives. As increased use of freezers would lead to greater energy consumption, the review was followed by an experimental assessment which found that the value and carbon dioxide emissions associated with the saved food far outweighed those associated with the additional energy. © 2013 Elsevier Ltd and IIR. All rights reserved
APOE genotype and cognitive change in young, middle-aged, and older adults living in the community.
We examined whether the apolipoprotein E (APOE) ε4 allele was associated with cognitive benefits in young adulthood and whether it reversed to confer cognitive deficits in later life ("antagonistic pleiotropy") in the absence of dementia-related neuropathology. We also tested whether the ε2 allele was associated with disadvantages in early adulthood but offered protection against cognitive decline in early old age. Eight-year cognitive change was assessed in 2,013 cognitively normal community-dwelling adults aged 20-24, 40-44, or 60-64 years at baseline. Although cognitive decline was associated with age, multilevel models contrasting the ε2 and ε4 alleles provided no evidence that the APOE genotype was related to cognitive change in any of the age groups. The findings suggest that in the absence of clinically salient dementia pathology, APOE ε2 and ε4 alleles do not exhibit antagonistic pleiotropy in relation to cognition between the ages of 20 and 72 years
Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression
The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.Molecular Psychiatry advance online publication, 4 April 2017; doi:10.1038/mp.2017.44.ALSPAC: Grant 102215/2/13/2 from The Wellcome Trust and grant MC_UU_12013-
/6 from the UK Medical Research Council. The University of Bristol also provides core
support for ALSPAC. LB receives funding as an Early Career Research Fellow from the
Leverhulme Trust. MRM is a member of the UK Centre for Tobacco and Alcohol Studies, a UK Clinical Research Council Public Health Research: Centre of Excellence.
Funding from British Heart Foundation, Cancer Research UK, Economic and Social
Research Council, Medical Research Council, and the National Institute for Health
Research, under the auspices of the UK Clinical Research Collaboration, is gratefully
acknowledged. ASPIS: EKBAN 97 from the General Secretariat of Research and
Technology, Greek Ministry of Development. ATP: Grants DP130101459,
DP160103160 and APP1082406 from the Australian Research Council and The
National Health and Medical Research Council of Australia. CHDS: Grant HRC 11/792
from the Health Research Council of New Zealand. CoFaMS: Grant APP1060524 to
BTB from the National Health and Medical Research Council of Australia. We
acknowledge the University of Adelaide for the provision of seed funding in support
of this project. COGA: Grant U10AA008401 from the National Institutes of Health,
NIAAA and NIDA. COGEND: National Institutes of Health grants P01CA089392 from
NCI and R01DA036583 from NIDA. DeCC: Grant G0701420 from the UK Medical
Research Council, and a UK MRC Population Health Scientist fellowship (G1002366)
and an MQ Fellows Award (MQ14F40) to Helen L Fisher. EPIC-Norfolk: Grants
G9502233, G0300128, C865/A2883 from the UK Medical Research Council and Cancer
Research UK. ESPRIT Montpellier: An unconditional grant from Novartis and from the
National Research Agency (ANR Project 07 LVIE004). G1219: A project grant from the
WT Grant Foundation and G120/635, a Career Development Award from the UK
Medical Research Council to Thalia Eley. The GENESiS project was supported by Grant
G9901258 from the UK Medical Research Council. This study presents independent
research part- funded by the National Institute for Health Research (NIHR) Biomedical
Research Centre at South London and Maudsley NHS Foundation Trust and King’s
College London. The views expressed are those of the author(s) and not necessarily
those of the NHS, the NIHR or the Department of Health. GAN12-France: Research
Protocol C0829 from INSERM; Research Protocol GAN12 from Assistance Publique des
Hôpitaux de Paris; ANR-11-IDEX- 0004 from Investissements d’Avenir program
managed by the ANR, and RTRS Sante Mentale from Fondation FondaMental.
GENESIS: Grant PHRC UF 7653 & ANR NEURO 2007 ‘GENESIS’ from CHU Montpellier &
Agence Nationale de la Recherche. Heart and Soul: Epidemiology Merit Review
Program from the Department of Veterans Affairs; National Institutes of Health grant
R01HL-079235 from NHLBI; Generalist Physician Faculty Scholars Program from the
Robert Woods Johnson foundation; Paul Beeson Faculty Scholars Program from the
American Federation for Aging Research; and a Young Investigator Award from the
Bran and Behavior Research Foundation. MARS: Grant LA 733/2-1 from German
Research Foundation (DFG) and the Federal Ministry for Education and Research as
part of the 'National Genome Research Network'. MLS: National Institutes of Health
grants R01 AA07065 and R37 AA07065 from NIAAA. MoodInFlame: Grant EU-FP7-
HEALTH-F2-2008-222963 from the European Union. Muenster Neuroimaging Study:
Grant FOR2107, DA1151/5-1 from the German Research Foundation (DFG). NEWMOOD: Grants LSHM-CT-2004-503474 from Sixth Framework Program of the
European Union; KTIA_NAP_13-1-2013-0001, KTIA_13_NAP-A-II/14 from National
Development Agency Hungarian Brain Research Program; KTIA_NAP_13-2-2015-0001
from MTA-SE-NAP B Genetic Brain Imaging Migraine Research Group, Hungarian
Academy of Sciences, Semmelweis University; support from Hungarian Academy of
Sciences, MTA-SE Neuropsychopharmacology and Neurochemistry Research Group;
and support from the National Institute for Health Research Manchester Biomedical
Research Centre. NESDA/NTR: The Netherlands Organization for Scientific Research
(NWO) and MagW/ZonMW grants Middelgroot-911-09-032, Spinozapremie 56-464-
14192, Geestkracht program of the Netherlands Organization for Health Research
and Development (ZonMW 10-000-1002), Center for Medical Systems Biology (CSMB,
NWO Genomics), Genetic influences on stability and change in psychopathology
from childhood to young adulthood (ZonMW 912-10-020), NBIC/BioAssist/RK
(2008.024), Biobanking and Biomolecular Resources Research Infrastructure (BBMRI
-NL, 184.021.007), VU University's Institute for Health and Care Research (EMGO+) and
Neuroscience Campus Amsterdam (NCA); the European Science Council (ERC
Advanced, 230374). Part of the genotyping and analyses were funded by the
Genetic Association Information Network (GAIN) of the Foundation for the National
Institutes of Health, Rutgers University Cell and DNA Repository (NIMH U24
MH068457-06), the Avera Institute, Sioux Falls, South Dakota (USA) and the National
Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants
1RC2 MH089951 and 1RC2 MH089995). PATH: Program Grant Number 179805 from
the National Health and Medical Research Council of Australia. POUCH: Grants
20FY01-38 and 20-FY04-37 of the Perinatal Epidemiologic Research Initiative Program
Grant from the March of Dimes Foundation; National Institutes of Health grant R01
HD34543 from NICHD and NINR; grant 02816-7 from the Thrasher Research
Foundation; and grant U01 DP000143-01 from the Centers for Disease Control and
Prevention. QIMRtwin: Grants 941177, 971232, 339450, 443011 from the National
Health and Medical Research Council of Australia; AA07535, AA07728, AA10249 from
US Public Health Service; National Institutes of Health grant K99DA023549-01A2 from
NIDA. Additional support was provided by Beyond Blue. SALVe 2001 and SALVe 2006:
Grants FO2012-0326, FO2013-0023, FO2014-0243 from The Brain Foundation
(Hjärnfonden); SLS-559921 from Söderström-Königska Foundation; 2015-00897 from
Swedish Council for Working Life and Social Research; and M15-0239 from Åke Wiberg's Foundation. Additional funding was provided by Systembolagets Råd för
Alkoholforskning, SRA and Svenska Spel Research Council. SEBAS: National Institutes
of Health grants R01 AG16790, R01 AG16661 and R56 AG01661 from NIA and grant
P2CHD047879 from NICHD; and additional financial support from the Graduate
School of Arts and Sciences at Georgetown University. SHIP/TREND: This work was
supported by the German Federal Ministry of Education and Research within the
framework of the e:Med research and funding concept (Integrament) Grant No.
01ZX1314E. Study of Health in Pomerania is part of the Community Medicine
Research net of the University of Greifswald, Germany, which is funded by the
Federal Ministry of Education and Research Grant Nos. 01ZZ9603, 01ZZ0103 and
01ZZ0403; the Ministry of Cultural Affairs; and the Social Ministry of the Federal State
of Mecklenburg-West Pomerania. Genome-wide data were supported by the Federal
Ministry of Education and Research Grant No. 03ZIK012 and a joint grant from
Siemens Healthcare, Erlangen, Germany and the Federal State of Mecklenburg-West
Pomerania. The Greifswald Approach to Individualised Medicine (GANI_MED) was
funded by the Federal Ministry of Education and Research Grant No. 03IS2061A and
the German Research Foundation Grant No. GR 1912/5-1. TRAILS: Grants GB-MW 940-
38-011, ZonMW Brainpower 100-001-004, Investment grant 175.010.2003.005, GBMaGW 480-07-001 and Longitudinal Survey and Panel Funding 481-08-013 from the
Netherlands Organization for Scientific Research (NWO). Additional funding was
provided by the Dutch Ministry of Justice, the European Science Foundation, BBMRINL and the participating centres (UMCG, RUG, Erasmus MC, UU, Radboud MC,
Parnassia Bavo group): VAHCS: Grants APP1063091, 1008271 and 1019887 from
Australia’s National Health and Medical Research Council of Australia (NHMRC)
Deep saltwater in Chalk of North-West Europe: origin, interface characteristics and development over geological time
Domestic Violence and Health Care: Opening Pandora¿s Box ¿ Challenges and Dilemmas
In this article we take a critical stance toward the rational progressive narrative
surrounding the integration of domestic violence within health care. Whilst changes in
recent UK policy and practice have resulted in several tangible benefits, it is argued that
there may be hidden dilemmas and challenges. We suggest that the medical model of care
and its discursive practices position women as individually accountable for domestic
violence-related symptoms and injuries. This may not only be ineffective in terms of
service provision but could also have the potential to reduce the political significance of
domestic violence as an issue of concern for all women. Furthermore, it is argued that the
use of specific metaphors enables practitioners to distance themselves from interactions
that may prove to be less comfortable and provide less than certain outcomes. Our analysis
explores the possibilities for change that might currently be available. This would
appear to involve a consideration of alternative discourses and the reformulation of power
relations and subject positions in health care
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