Dark homogenous fungal-based layers called biofinishes and vegetable oils are keyingredients of an innovative wood protecting system. The aim of this study was todetermine which of the vegetable oils that have been used to generate biofinishes onwood will provide carbon and energy for the biofinish-inhabiting fungus Aureobasidiummelanogenum, and to determine the effect of the oil type and the amount of oil on thecell yield. Aureobasidium melanogenum was cultivated in shake flasks with differenttypes and amounts of carbon-based nutrients. Oil-related total cell and colony-formingunit growth were demonstrated in suspensions with initially 1% raw linseed,stand linseed, and olive oil. Oil-related cell growth was also demonstrated with rawlinseed oil, using an initial amount of 0.02% and an oil addition during cultivation. Nilered staining showed the accumulation of fatty acids inside cells grown in the presenceof oil. In conclusion, each tested vegetable oil was used as carbon and energysource by A. melanogenum. The results indicated that stand linseed oil provides lesscarbon and energy than olive and raw linseed oil. This research is a fundamental stepin unraveling the effects of vegetable oils on biofinish formation.
MULTIFILE
Insulin sensitivity and metabolic flexibility decrease in response to bed rest, but the temporal and causal adaptations in human skeletal muscle metabolism are not fully defined. Here, we use an integrative approach to assess human skeletal muscle metabolism during bed rest and provide a multi-system analysis of how skeletal muscle and the circulatory system adapt to short- and long-term bed rest (German Clinical Trials: DRKS00015677). We uncover that intracellular glycogen accumulation after short-term bed rest accompanies a rapid reduction in systemic insulin sensitivity and less GLUT4 localization at the muscle cell membrane, preventing further intracellular glycogen deposition after long-term bed rest. We provide evidence of a temporal link between the accumulation of intracellular triglycerides, lipotoxic ceramides, and sphingomyelins and an altered skeletal muscle mitochondrial structure and function after long-term bed rest. An intracellular nutrient overload therefore represents a crucial determinant for rapid skeletal muscle insulin insensitivity and mitochondrial alterations after prolonged bed rest.
Skeletal muscle-related symptoms are common in both acute coronavirus disease (Covid)-19 and post-acute sequelae of Covid-19 (PASC). In this narrative review, we discuss cellular and molecular pathways that are affected and consider these in regard to skeletal muscle involvement in other conditions, such as acute respiratory distress syndrome, critical illness myopathy, and post-viral fatigue syndrome. Patients with severe Covid-19 and PASC suffer from skeletal muscle weakness and exercise intolerance. Histological sections present muscle fibre atrophy, metabolic alterations, and immune cell infiltration. Contributing factors to weakness and fatigue in patients with severe Covid-19 include systemic inflammation, disuse, hypoxaemia, and malnutrition. These factors also contribute to post-intensive care unit (ICU) syndrome and ICU-acquired weakness and likely explain a substantial part of Covid-19-acquired weakness. The skeletal muscle weakness and exercise intolerance associated with PASC are more obscure. Direct severe acute respiratory syndrome coronavirus (SARS-CoV)-2 viral infiltration into skeletal muscle or an aberrant immune system likely contribute. Similarities between skeletal muscle alterations in PASC and chronic fatigue syndrome deserve further study. Both SARS-CoV-2-specific factors and generic consequences of acute disease likely underlie the observed skeletal muscle alterations in both acute Covid-19 and PASC.
