2,824 research outputs found

    24-Hour sleep/wake patterns in healthy elderly persons

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    The purpose of this study was to examine the 24-hour sleep/wake patterns of healthy elderly persons. Data was obtained from 14 elderly subjects who wore a wrist actigraph for 48 hours and completed an activity diary during the monitoring period. Although subjects spent slightly more than 7.5 hours in bed at night, they were asleep for just over 6 hours. Subjects did not have trouble falling asleep, but once asleep, had trouble remaining asleep. All subjects took one or more naps during the recording period, but daytime naps composed only a small fraction of their total sleep time. Total duration of daytime sleep averaged 59.8 minutes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31596/1/0000525.pd

    Factors associated with transition from community settings to hospital as place of death for adults aged 75 years or older: a population-based mortality follow-back survey

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    Objective: To identify factors associated with end of life (EoL) transition from usual place of care to hospital as place of death for people aged 75 years or older (75+). Design: Population-based mortality follow-back survey. Setting: Deaths over six months in 2012 in two unitary authorities in England, covering 800 square miles with over one million residents. Participants: A random sample of people aged 75+ who died in a care home or hospital and all those who died at home or in a hospice unit. Cases were identified from death registrations. The person who registered the death (a relative for 98.9%) completed the survey. Measurements: Our main outcome was EoL transition to hospital as place of death versus no EoL transition to hospital. We used multivariable modified Poisson regression to examine factors (illness, demographic and environmental) related to EoL transition to hospital. Results: 443/882 (50.2%) responded, describing the care received by people who died from mostly non-malignant conditions (76.3%) at mean age 87.4 years (SD= 6.4). 32.3% transitioned to hospital and died there (n=146). Transition was more likely in respiratory disease compared to cancer (Prevalence Ratio [PR] =2.07, 95%CI 1.42- 3.01) and for people with severe breathlessness (PR=1.96, 95%CI 1.12-3.43). Transition was less likely if EoL preferences had been discussed with a healthcare professional (PR=0.60, 95%CI 0.42-0.88) and when there was a key healthcare professional (PR=0.74, 95%CI 0.58-0.95). Conclusion: To reduce EoL transition to hospital for older people this study suggests a need to improve the symptom management of breathlessness in the community and better access to a key healthcare professional skilled in coordinating care, communication, facilitating complex discussions and in planning for future care

    Understanding the science of portion control and the art of downsizing

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    Offering large portions of high-energy-dense (HED) foods increases overall intake in children and adults. This is known as the portion size effect (PSE). It is robust, reliable and enduring. Over time, the PSE may facilitate overeating and ultimately positive energy balance. Therefore, it is important to understand what drives the PSE and what might be done to counter the effects of an environment promoting large portions, especially in children. Explanations for the PSE are many and diverse, ranging from consumer error in estimating portion size to simple heuristics such as cleaning the plate or eating in accordance with consumption norms. However, individual characteristics and hedonic processes influence the PSE, suggesting a more complex explanation than error or heuristics. Here PSE studies are reviewed to identify interventions that can be used to downsize portions of HED foods, with a focus on children who are still learning about social norms for portion size. Although the scientific evidence for the PSE is robust, there is still a need for creative downsizing solutions to facilitate portion control as children and adolescents establish their eating habits

    Prevention of Alzheimer's disease in high risk groups: statin therapy in subjects with PSEN1 mutations or heterozygosity for apolipoprotein E epsilon 4

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    Because cerebrospinal fluid (CSF) abnormalities in presymptomatic subjects with PSEN1 (presenilin 1) mutations may be observed 4 to 12 years prior to the estimated age at onset, it is possible to test putative therapies on the CSF analytes that correlate with neurodegeneration during this presymptomatic window of clinical opportunity. It is also possible to test the same therapy on a comparison group with increased risk status conferred by both hyperlipidemia and heterozygosity for apolipoprotein Eε4. To our knowledge, the only putative therapy thus far tested in such a common design has been statin therapy. The results of these tests show increases in soluble amyloid precursor protein (sAPP)α correlating with statin-induced decreases in serum cholesterol levels in the non-PSEN1 subjects. This result could be one functional correlate for part of the substantial risk reduction for late onset Alzheimer\u27s disease recently reported in the Rotterdam study, a large, long-term prospective statin trial. Statin therapy significantly decreased both sAPPα and sAPPβ in presymptomatic PSEN1 subjects. Initially, elevated phospho-tau levels in PSEN1 subjects did not further increase during the 2 to 3 years of statin therapy, possibly indicative of a prophylactic effect. These results suggest that large and longer term trials of statin therapy correlating changes in CSF biomarker levels with clinical course may be warranted in both presymptomatic PSEN1 and non-PSEN1 subjects

    What is the impact of population ageing on the future provision of end-of-life care? Population-based projections of place of death.

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    BACKGROUND: Population ageing represents a global challenge for future end-of-life care. Given new trends in place of death, it is vital to examine where the rising number of deaths will occur in future years and implications for health and social care. AIM: To project where people will die from 2015 to 2040 across all care settings in England and Wales. DESIGN: Population-based trend analysis and projections using simple linear modelling. Age- and gender-specific proportions of deaths in hospital, care home, home, hospice and 'other' were applied to numbers of expected future deaths. Setting/population: All deaths (2004-2014) from death registration data and predicted deaths (2015-2040) from official population forecasts in England and Wales. RESULTS: Annual deaths are projected to increase from 501,424 in 2014 (38.8% aged 85 years and over) to 635,814 in 2040 (53.6% aged 85 years and over). Between 2004 and 2014, proportions of home and care home deaths increased (18.3%-22.9% and 16.7%- 21.2%) while hospital deaths declined (57.9%-48.1%). If current trends continue, numbers of deaths in care homes and homes will increase by 108.1% and 88.6%, with care home the most common place of death by 2040. If care home capacity does not expand and additional deaths occur in hospital, hospital deaths will start rising by 2023. CONCLUSION: To sustain current trends, end-of-life care provision in care homes and the community needs to double by 2040. An infrastructure across care settings that supports rising annual deaths is urgently needed; otherwise, hospital deaths will increase.The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: This work is independent research funded by Cicely Saunders International and The Atlantic Philanthropies (grant number 24610). This research was supported by the Collaboration for Leadership in Applied Health Research and Care (CLAHRC) South London, which is part of the National Institute for Health Research (NIHR), and is a partnership between King’s Health Partners, St. George’s, University London and St George’s Healthcare NHS Trust. I.J.H. is an NIHR Senior Investigator. C.J.E. is funded by a Health Education England (HEE)/NIHR Senior Clinical Lectureship. B.G. is funded by the Calouste Gulbenkian Foundation. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health

    Discovery of the 2010 Eruption and the Pre-Eruption Light Curve for Recurrent Nova U Scorpii

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    We report the discovery by B. G. Harris and S. Dvorak on JD 2455224.9385 (2010 Jan 28.4385 UT) of the predicted eruption of the recurrent nova U Scorpii (U Sco). We also report on 815 magnitudes (and 16 useful limits) on the pre-eruption light curve in the UBVRI and Sloan r' and i' bands from 2000.4 up to 9 hours before the peak of the January 2010 eruption. We found no significant long-term variations, though we did find frequent fast variations (flickering) with amplitudes up to 0.4 mag. We show that U Sco did not have any rises or dips with amplitude greater than 0.2 mag on timescales from one day to one year before the eruption. We find that the peak of this eruption occurred at JD 2455224.69+-0.07 and the start of the rise was at JD 2455224.32+-0.12. From our analysis of the average B-band flux between eruptions, we find that the total mass accreted between eruptions is consistent with being a constant, in agreement with a strong prediction of nova trigger theory. The date of the next eruption can be anticipated with an accuracy of +-5 months by following the average B-band magnitudes for the next ~10 years, although at this time we can only predict that the next eruption will be in the year 2020+-2.Comment: Astronomical Journal submitted, 36 pages, 3 figures, full table

    Aberrantly Expressed Genes in HaCaT Keratinocytes Chronically Exposed to Arsenic Trioxide

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    Inorganic arsenic is a known environmental toxicant and carcinogen of global public health concern. Arsenic is genotoxic and cytotoxic to human keratinocytes. However, the biological pathways perturbed in keratinocytes by low chronic dose inorganic arsenic are not completely understood. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide. The expression of 4 up-regulated genes and 1 down-regulated gene were confirmed by qRT-PCR. The up-regulated genes were AKR1C3 (Aldo-Keto Reductase family 1, member C3), IGFL1 (Insulin Growth Factor-Like family member 1), IL1R2 (Interleukin 1 Receptor, type 2), and TNFSF18 (Tumor Necrosis Factor [ligand] SuperFamily, member 18) and down-regulated gene was RGS2 (Regulator of G-protein Signaling 2). The observed over expression of TNFSF18 (167 fold) coupled with moderate expression of IGFL1 (3.1 fold), IL1R2 (5.9 fold) and AKR1C3 (9.2 fold) with a decreased RGS2 (2.0 fold) suggests that chronic arsenic exposure could produce sustained levels of TNF with modulation by an IL-1 analogue resulting in chronic immunologic insult. A concomitant decrease in growth inhibiting gene (RGS2) and increase in AKR1C3 may contribute to chronic inflammation leading to metaplasia, which may eventually lead to carcinogenicity in the skin keratinocytes. Also, increased expression of IGFL1 may trigger cancer development and progression in HaCaT keratinocytes
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