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1.
  • Munobwa, Jimmy, et al. (författare)
  • Coping methods and satisfaction with working from home in academic settings during the COVID-19 pandemic
  • 2022
  • Ingår i: International Journal of Environmental Research and Public Health. - : MDPI. - 1661-7827 .- 1660-4601. ; 19:19
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper, we examined how university staff and students coped with challenges related to working or studying from home during the COVID-19 pandemic, and the level of satisfaction with working from home. An online survey was conducted among faculty, staff, and students at universities in 24 countries (n = 674). The results show that over 80% of the respondents used multiple coping methods. Three clusters of coping methods were generated through factor analysis: (1) social and health factor, with focus on personal health and the social surrounding, (2) activity factor, i.e., being busy with work or studies, finding up-to-date information about COVID-19, while thinking about what one could do rather than what one could not do, and (3) public health factor, which meant trusting health authorities while avoiding misinformation from sources such as social media. Furthermore, 56% of the respondents were very or somewhat satisfied with working from home. Differences in the methods of coping and satisfaction with working from home highlight the need for employers to prepare for working from home beyond the COVID-19 pandemic.
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2.
  • Soylu Kucharz, Rana, et al. (författare)
  • Mutant huntingtin expression in the hypothalamus promotes ventral striatal neuropathology
  • 2023
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Huntington’s disease is a fatal neurodegenerative disorder caused by an expanded CAG triplet repeat in the huntingtin (HTT) gene. Previous research focused on neuropathology in the striatum and its association with a typical movement disorder. Direct effects of mutant HTT (mHTT) in the striatum may cause neuropathology, although non-cell autonomous effects have also been suggested. Important non-motor features of HD include psychiatric symptoms and metabolic dysfunction, which may be linked to hypothalamic neuropathology. As hypothalamic neurons project to the ventral striatum, we hypothesized that expression of mHTT in the hypothalamus leads to disrupted neurotransmission in the ventral striatum and causes pathology. The overall aim of this study was to investigate the impact of mHTT expression in the hypothalamus on ventral striatal neuropathology and its contribution to non-HD motor symptoms. We demonstrate that selective expression of mHTT in the hypothalamus leads to the loss of dopamine and cAMP-regulated phosphoprotein (DARPP-32) immunopositive neurons in the ventral striatum in mice. Contrary to the effects of direct expression of mHTT in the hypothalamus, selective overexpression of mHTT in the ventral striatum does not affect body weight. Selective expression of mHTT in the ventral striatum leads to mHTT inclusion formation and loss of DARPP-32 neurons without affecting motor activity or anxiety-like behavior. We show that DARPP-32 neuron loss in the ventral striatum is recapitulated in the R6/2 mouse model of HD. Chemogenetic activation of hypothalamic neurons projecting to the ventral striatum had a blunted response in the R6/2 mice compared to wild-type mice, indicating a disrupted hypothalamus-ventral striatal circuitry. In summary, the expression of mHTT in the hypothalamus may impact the development of ventral striatal pathology in mice. This opens the possibility that non-cell-autonomous effects in the reward circuitry play a role in HD.
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