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- Meyer, S, et al.
(författare)
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Somatosensory Impairments in the Upper Limb Poststroke: Distribution and Association With Motor Function and Visuospatial Neglect
- 2016
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Ingår i: Neurorehabilitation and neural repair. - : SAGE Publications. - 1552-6844 .- 1545-9683. ; 30:8, s. 731-742
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Tidskriftsartikel (refereegranskat)abstract
- Background. A thorough understanding of the presence of different upper-limb somatosensory deficits poststroke and the relation with motor performance remains unclear. Additionally, knowledge about the relation between somatosensory deficits and visuospatial neglect is limited. Objective. To investigate the distribution of upper-limb somatosensory impairments and the association with unimanual and bimanual motor outcomes and visuospatial neglect. Methods. A cross-sectional observational study was conducted, including 122 patients within 6 months after stroke (median = 82 days; interquartile range = 57-133 days). Somatosensory measurement included the Erasmus MC modification of the (revised) Nottingham Sensory Assessment (Em-NSA), Perceptual Threshold of Touch (PTT), thumb finding test, 2-point discrimination, and stereognosis subscale of the NSA. Upper-limb motor assessment comprised the Fugl-Meyer assessment, motricity index, Action Research Arm Test, and Adult-Assisting Hand Assessment Stroke. Screening for visuospatial neglect was performed using the Star Cancellation Test. Results. Upper-limb somatosensory impairments were common, with prevalence rates ranging from 21% to 54%. Low to moderate Spearman ρ correlations were found between somatosensory and motor deficits ( r = 0.22-0.61), with the strongest associations for PTT ( r = 0.56-0.61) and stereognosis ( r = 0.51-0.60). Visuospatial neglect was present in 27 patients (22%). Between-group analysis revealed somatosensory deficits that occurred significantly more often and more severely in patients with visuospatial neglect ( P < .05). Results showed consistently stronger correlations between motor and somatosensory deficits in patients with visuospatial neglect ( r = 0.44-0.78) compared with patients without neglect ( r = 0.08-0.59). Conclusions. Somatosensory impairments are common in subacute patients poststroke and are related to motor outcome. Visuospatial neglect was associated with more severe upper-limb somatosensory impairments.
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- Ruppert, Philip M. M., et al.
(författare)
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Fasting induces ANGPTL4 and reduces LPL activity in human adipose tissue
- 2020
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Ingår i: Molecular Metabolism. - : Elsevier. - 2212-8778. ; 40
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Studies in mice have shown that the decrease in lipoprotein lipase (LPL) activity in adipose tissue upon fasting is mediated by induction of the inhibitor ANGPTL4. Here, we aimed to validate this concept in humans by determining the effect of a prolonged fast on ANGPTL4 and LPL gene and protein expression in human subcutaneous adipose tissue.Methods: Twenty-three volunteers ate a standardized meal at 18.00 h and fasted until 20.00 h the next day. Blood was drawn and periumbilical adipose tissue biopsies were collected 2 h and 26 h after the meal.Results: Consistent with previous mouse data, LPL activity in human adipose tissue was significantly decreased by fasting (−60%), concurrent with increased ANGPTL4 mRNA (+90%) and decreased ANGPTL8 mRNA (−94%). ANGPTL4 protein levels in adipose tissue were also significantly increased by fasting (+46%), whereas LPL mRNA and protein levels remained unchanged. In agreement with the adipose tissue data, plasma ANGPTL4 levels increased upon fasting (+100%), whereas plasma ANGPTL8 decreased (−79%). Insulin, levels of which significantly decreased upon fasting, downregulated ANGPTL4 mRNA and protein in primary human adipocytes. By contrast, cortisol, levels of which significantly increased upon fasting, upregulated ANGPTL4 mRNA and protein in primary human adipocytes as did fatty acids.Conclusion: ANGPTL4 levels in human adipose tissue are increased by fasting, likely via increased plasma cortisol and free fatty acids and decreased plasma insulin, resulting in decreased LPL activity.
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