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Sökning: WFRF:(Walden Camilla)

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1.
  • Carlsson, Christer, et al. (författare)
  • Go Vendla Go! Creating a Digital Coach for the Young Elderly
  • 2017
  • Ingår i: INFORMATION SYSTEMS, EMCIS 2017. - Cham : Springer. - 9783319659305 - 9783319659299 ; , s. 204-209
  • Konferensbidrag (refereegranskat)abstract
    • The proportion of ageing citizens is high and increasing in most EU countries and there is a growing political pressure to make sure that the costs for the elderly care programs do not grow out of bounds. The focus of the ageing population programs is at the 75+ age group. The younger age group - the "young elderly" that is the focus in our research - does not get much attention. Recently, we have noticed a growing insight that preventive programs could be helpful as healthier young elderly will help produce healthier seniors (the 75 + age group) which over time will have significant effects on the costs for health and social care for the ageing population. Our study is a synergistic combination of two timely research areas: digitalisation and the ageing population. The focus combination of digital wellness services and the young elderly is unique. We build on a research program that is operating since January 2014. Our current research in progress aims at finding out how a digital coach - a personal trainer called Vendla - can be worked out for digital wellness services.
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2.
  • Scheele, Camilla, et al. (författare)
  • Altered regulation of the PINK1 locus: a link between Type 2 diabetes and neurodegeneration?
  • 2007
  • Ingår i: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 21:13, s. 3653-3665
  • Tidskriftsartikel (refereegranskat)abstract
    • Mutations in PINK1 cause the mitochondrial-related neurodegenerative disease Parkinson’s. Here we investigate whether obesity, type 2 diabetes, or inactivity alters transcription from the PINK1 locus. We utilized a cDNA-array and quantitative real-time PCR for gene expression analysis of muscle from healthy volunteers following physical inactivity, and muscle and adipose tissue from nonobese or obese subjects with normal glucose tolerance or type 2 diabetes. Functional studies of PINK1 were performed utilizing RNA interference in cell culture models. Following inactivity, the PINK1 locus had an opposing regulation pattern (PINK1 was down-regulated while natural antisense PINK1 was up-regulated). In type 2 diabetes skeletal muscle, all transcripts from the PINK1 locus were suppressed and gene expression correlated with diabetes status. RNA interference of PINK1 in human neuronal cell lines impaired basal glucose uptake. In adipose tissue, mitochondrial gene expression correlated with PINK1 expression although remained unaltered following siRNA knockdown of Pink1 in primary cultures of brown preadipocytes. In conclusion, regulation of the PINK1 locus, previously linked to neurodegenerative disease, is altered in obesity, type 2 diabetes and inactivity, while the combination of RNAi experiments and clinical data suggests a role for PINK1 in cell energetics rather than in mitochondrial biogenesis.
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