| 1. |
- Korpela, Kalevi M., et al.
(författare)
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Environmental Strategies of Affect Regulation and Their Associations With Subjective Well-Being
- 2018
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Ingår i: Frontiers in Psychology. - : Frontiers Media SA. - 1664-1078. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Environmental strategies of affect regulation refer to the use of natural and urban socio-physical settings in the service of regulation. We investigated the perceived use and efficacy of environmental strategies for regulation of general affect and sadness, considering them in relation to other affect regulation strategies and to subjective well-being. Participants from Australia, Finland, Germany, Great Britain, Italy, India, the Netherlands, Portugal, and Sweden (N = 507) evaluated the frequency of use and perceived efficacy of affect regulation strategies using a modified version of the Measure of Affect Regulation Styles (MARS). The internet survey also included the Satisfaction with Life Scale (SWLS), emotional well-being items from the RAND 36-Item Health Survey, and a single-item measure of perceived general health. Environmental regulation formed a separate factor of affect regulation in the exploratory structural equation models (ESEM). Although no relations of environmental strategies with emotional well-being were found, both the perceived frequency of use and efficacy of environmental strategies were positively related to perceived health. Moreover, the perceived efficacy of environmental strategies was positively related to life satisfaction in regulating sadness. The results encourage more explicit treatment of environmental strategies in research on affect regulation.
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| 2. |
- Picca, Anna, et al.
(författare)
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Altered Expression of Mitoferrin and Frataxin, Larger Labile Iron Pool and Greater Mitochondrial DNA Damage in the Skeletal Muscle of Older Adults
- 2020
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Ingår i: Cells. - : MDPI AG. - 2073-4409. ; 9:12
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Tidskriftsartikel (refereegranskat)abstract
- Mitochondrial dysfunction and iron (Fe) dyshomeostasis are invoked among the mechanisms contributing to muscle aging, possibly via a detrimental mitochondrial-iron feed-forward loop. We quantified the labile Fe pool, Fe isotopes, and the expression of mitochondrial Fe handling proteins in muscle biopsies obtained from young and older adults. The expression of key proteins of mitochondrial quality control (MQC) and the abundance of the mitochondrial DNA common deletion (mtDNA(4977)) were also assessed. An inverse association was found between total Fe and the heavier Fe isotope (Fe-56), indicating an increase in labile Fe abundance in cells with greater Fe content. The highest levels of labile Fe were detected in old participants with a Short Physical Performance Battery (SPPB) score <= 7 (low-functioning, LF). Protein levels of mitoferrin and frataxin were, respectively, higher and lower in the LF group relative to young participants and older adults with SPPB scores >= 11 (high-functioning, HF). The mtDNA(4977) relative abundance was greater in old than in young participants, regardless of SPPB category. Higher protein levels of Pink1 were detected in LF participants compared with young and HF groups. Finally, the ratio between lipidated and non-lipidated microtubule-associated protein 1A/1B-light chain 3 (i.e., LC3B II/I), as well as p62 protein expression was lower in old participants regardless of SPPB scores. Our findings indicate that cellular and mitochondrial Fe homeostasis is perturbed in the aged muscle (especially in LF older adults), as reflected by altered levels of mitoferrin and frataxin, which, together with MQC derangements, might contribute to loss of mtDNA stability.
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