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- Badinlou, F., et al.
(författare)
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Impairments following COVID-19 infection: manifestations and investigations of related factors
- 2023
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Ingår i: Scientific Reports. - 2045-2322. ; 13:1
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Tidskriftsartikel (refereegranskat)abstract
- The COVID-19 pandemic had a major global impact on the health and wellbeing for many individuals. Even though the infection rates have gone down due to the availability of vaccines, the consequences of the disease are still present due to persistent symptoms among individuals. The aim of the current study was to map long-term impairments in individuals infected with COVID-19 by applying the framework of the World Health Organization's International Classification of Functioning, Disability and Health (ICF) and also investigate the factors related to the context of an individual's life influencing the impairments. A web-survey that targeted individuals that had been infected with COVID-19 was used. The survey included a range of measures covering contextual factors and factors related to body functions and structures and post-COVID impairments. A total of 501 individuals were included in the study (with a mean age of 47.6 years). 96% of the respondents reported at least one moderate-to-severe impairment due to COVID-19 infection and the most frequent one was fatigue. In that, 79.6% and 86.9% of the study sample reported moderate-to-severe brain fatigue and tiredness or lack of energy, respectively. Severity of COVID-19 infection appeared as the strongest risk factor for post-COVID impairments. Based on the results, interventions can be tailored to help individuals with post-COVID-19 condition. This could be one way lessening the effect of COVID-19 on health care and society as a whole.
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| 2. |
- Petkevicius, K., et al.
(författare)
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TLCD1 and TLCD2 regulate cellular phosphatidylethanolamine composition and promote the progression of non-alcoholic steatohepatitis
- 2022
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1
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Tidskriftsartikel (refereegranskat)abstract
- The regulation of cellular phosphatidylethanolamine (PE) acyl chain composition is poorly understood. Here, the authors show that TLCD1 and TLCD2 proteins mediate the formation of monounsaturated fatty acid-containing PE species and promote the progression of non-alcoholic steatohepatitis. The fatty acid composition of phosphatidylethanolamine (PE) determines cellular metabolism, oxidative stress, and inflammation. However, our understanding of how cells regulate PE composition is limited. Here, we identify a genetic locus on mouse chromosome 11, containing two poorly characterized genes Tlcd1 and Tlcd2, that strongly influences PE composition. We generated Tlcd1/2 double-knockout (DKO) mice and found that they have reduced levels of hepatic monounsaturated fatty acid (MUFA)-containing PE species. Mechanistically, TLCD1/2 proteins act cell intrinsically to promote the incorporation of MUFAs into PEs. Furthermore, TLCD1/2 interact with the mitochondria in an evolutionarily conserved manner and regulate mitochondrial PE composition. Lastly, we demonstrate the biological relevance of our findings in dietary models of metabolic disease, where Tlcd1/2 DKO mice display attenuated development of non-alcoholic steatohepatitis compared to controls. Overall, we identify TLCD1/2 proteins as key regulators of cellular PE composition, with our findings having broad implications in understanding and treating disease.
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