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- Bjursell, Cecilia, 1970-, et al.
(författare)
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Lifelong Learning Through Context Collapse : Higher education Teachers’ Narratives About Online education During The Pandemic
- 2022
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Ingår i: Proceedings of INTED2022 Conference 7th-8th March 2022. - : IATED. - 9788409377589 ; , s. 2632-2641
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Konferensbidrag (refereegranskat)abstract
- The COVID-19 pandemic has elicited a shift from campus classrooms to distance education in higher education worldwide, shaping not only students’ experiences, but also those of teachers, especially those who never have taught online. In addition, the pandemic created a meta-context that has positioned distance education as something different from previous efforts. This study aimed to investigate higher education teachers’ experiences during the transition from classroom to online teaching by using a collective auto-ethnography method based on 13 personal stories from Swedish faculty. For the abductive approach in the analysis, a framework that combines lifelong learning theory with the context collapse concept has been applied. The disjuncture that the pandemic has elicited created a situation in which teachers had to make sense of the fact that their previous experiences did not completely fit the new situation. Context collapse, a term used to describe encounters with many audiences in social media, has been introduced to highlight the clash between professional and private contexts in online educational platforms. Based on lifelong learning theories, we suggest that context collapse should be examined in terms of how it can help improve higher education, as it holds the potential to include the entire person – body and mind – in education.
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| 3. |
- Bjursell, Mikael, 1977, et al.
(författare)
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Acutely reduced locomotor activity is a major contributor to Western diet-induced obesity in mice
- 2008
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Ingår i: American Journal of Physiology-Endocrinology and Metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 294:2
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to investigate the short- and long-term effects of a high-fat Western diet (WD) on intake, storage, expenditure, and fecal loss of energy as well as effects on locomotor activity and thermogenesis. WD for only 24 h resulted in a marked physiological shift in energy homeostasis, including increased body weight gain, body fat, and energy expenditure (EE) but an acutely lowered locomotor activity. The acute reduction in locomotor activity was observed after only 3–5 h on WD. The energy intake and energy absorption were increased during the first 24 h, lower after 72 h, and normalized between 7 and 14 days on WD compared with mice given chow diet. Core body temperature and EE was increased between 48 and 72 h but normalized after 21 days on WD. These changes paralleled plasma T3 levels and uncoupling protein-1 expression in brown adipose tissue. After 21 days of WD, energy intake and absorption, EE, and body temperature were normalized. In contrast, the locomotor activity was reduced and body weight gain was increased over the entire 21-day study period on WD. Calculations based on the correlation between locomotor activity and EE in 2-h intervals at days 21–23 indicated that a large portion of the higher body weight gain in the WD group could be attributed to the reduced locomotor activity. In summary, an acute and persisting decrease in locomotor activity is most important for the effect of WD on body weight gain and obesity in mice.
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| 4. |
- Bjursell, Mikael, 1977, et al.
(författare)
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Deletion of Gpr55 Results in Subtle Effects on Energy Metabolism, Motor Activity and Thermal Pain Sensation
- 2016
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Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 11:12
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Tidskriftsartikel (refereegranskat)abstract
- The G-protein coupled receptor 55 (GPR55) is activated by cannabinoids and non-cannabinoid molecules and has been speculated to play a modulatory role in a large variety of physiological and pathological processes, including in metabolically perturbed states. We therefore generated male mice deficient in the gene coding for the cannabinoid/lysophosphatidylinositol (LPI) receptor Gpr55 and characterized them under normal dietary conditions as well as during high energy dense diet feeding followed by challenge with the CB1 receptor antagonist/GPR55 agonist rimonabant. Gpr55 deficient male mice (Gpr55 KO) were phenotypically indistinguishable from their wild type (WT) siblings for the most part. However, Gpr55 KO animals displayed an intriguing nocturnal pattern of motor activity and energy expenditure (EE). During the initial 6 hours of the night, motor activity was significantly elevated without any significant effect observed in EE. Interestingly, during the last 6 hours of the night motor activity was similar but EE was significantly decreased in the Gpr55 KO mice. No significant difference in motor activity was detected during daytime, but EE was lower in the Gpr55 KO compared to WT mice. The aforementioned patterns were not associated with alterations in energy intake, daytime core body temperature, body weight (BW) or composition, although a non-significant tendency to increased adiposity was seen in Gpr55 KO compared to WT mice. Detailed analyses of daytime activity in the Open Field paradigm unveiled lower horizontal activity and rearing time for the Gpr55 KO mice. Moreover, the Gpr55 KO mice displayed significantly faster reaction time in the tail flick test, indicative of thermal hyperalgesia. The BW-decreasing effect of rimonabant in mice on long-term cafeteria diet did not differ between Gpr55 KO and WT mice. In conclusion, Gpr55 deficiency is associated with subtle effects on diurnal/nocturnal EE and motor activity behaviours but does not appear per se critically required for overall metabolism or behaviours.
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| 6. |
- Bjursell, Mikael, 1977
(författare)
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Growth Hormone and Melanin-Concentrating Hormone receptor in the regulation of energy balance and metabolism
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Energy homeostasis ? the balance of energy intake, expenditure, and storage ? is controlled by autonomic regulation originating in the hypothalamus and the brain stem, which receive input from the periphery. Upon receiving signals from the periphery, centres in the central nervous system (CNS) react through endocrine or neuronal responses to maintain a steady balance. Growth hormone (GH) and melanin-concentrating hormone (MCH) act in the CNS to influence the energy balance and may be connected to the peripheral signals ghrelin and leptin. The overall aim of this thesis was to investigate how these different hormonal systems interact. To investigate the metabolic role of GH in the CNS, transgenic mice that overexpress bovine GH in the CNS (GFAP-bGH) were studied. GFAP-bGH mice have higher food intake and body weight and are obese compared with wild-type (WT) mice. Moreover, GFAP-bGH mice had hyperinsulinemia, pancreas islet hyperplasia, and dyslipidemia, but no changes in energy expenditure were observed. Thus, GH is an orexigenic signal in the CNS that leads to obesity and alters insulin and blood lipid profiles. Mice deficient in the gene encoding GHr (GHr KO) were injected in the CNS with ghrelin to study whether the orexigenic signal from ghrelin is dependent on functional GH signalling. The stimulatory effect of ghrelin on food intake was blunted in GHr KO mice, which suggests that the effects of ghrelin on food intake involve the central GH/GHr system. Furthermore, GHr KO mice were growth retarded and obese with higher leptin and corticosterone levels, low insulin and glucose levels and altered circulating lipids. Functional GH signalling is thus required for normal carbohydrate metabolism and lipid biology. The orexigenic neuropeptide MCH may also be involved in ghrelin-induced food intake and GH secretion. Food intake of mice that were deficient in the gene encoding MCHr (MCHr KO) and were injected in the CNS with ghrelin was similar to that of ghrelin injected WT mice, which suggests that MCHr is not required for the stimulating effect of ghrelin on food intake. But ghrelin had no effect on pituitary GH expression in MCHr KO mice, which suggests that MCHr is involved in ghrelin-mediated GH expression. Furthermore, MCHr is important for the acute effect of intracerebroventricular ghrelin on serum insulin but not on corticosterone levels. Thus, functional MCHr is required for the effects of ghrelin on GH expression and insulin secretion. Since leptin and MCH act in common pathways in the hypothalamus to regulate energy balance, leptin-deficient MCHr KO (MCHr KO ob/ob) mice were studied to investigate the importance of MCHr on the phenotype of ob/ob mice. MCHr KO ob/ob mice were similar to ob/ob mice concerning body weight, food intake, hepatic steatosis, blood lipid profile, and energy expenditure. But normal glucose tolerance and markedly reduced insulin levels were observed in MCHr KO ob/ob mice, indicating improved insulin sensitivity. MCHr KO ob/ob mice had higher locomotor activity, improved core body temperature regulation, and reduced corticosterone levels. Thus, MCHr may be involved in direct or secondary signalling cascades that lead to changes in insulin sensitivity, locomotor activity, and blood serum parameters. In conclusion, GH and MCHr play important roles in the CNS in regulating energy balance, including effects on food intake, body weight, obesity, and circulating endocrine signals.
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| 9. |
- Bjursell, Mikael, 1977, et al.
(författare)
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Opposing effects of adiponectin receptors 1 and 2 on energy metabolism
- 2007
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Ingår i: DIABETES. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 56:3, s. 583-593
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Tidskriftsartikel (refereegranskat)abstract
- The adipocyte-derived hormone adiponectin regulates glucose and lipid metabolism and influences the risk for developing obesity, type 2 diabetes, and cardiovascular disease. Adiponectin binds to two different seven-transmembrane domain receptors termed AdipoR1 and AdipoR2. To study the physiological importance of these receptors, AdipoR1 gene knockout mice (AdipoR1−/−) and AdipoR2 gene knockout mice (AdipoR2−/−) were generated. AdipoR1−/− mice showed increased adiposity associated with decreased glucose tolerance, spontaneous locomotor activity, and energy expenditure. However, AdipoR2−/− mice were lean and resistant to high-fat diet–induced obesity associated with improved glucose tolerance and higher spontaneous locomotor activity and energy expenditure and reduced plasma cholesterol levels. Thus, AdipoR1 and AdipoR2 are clearly involved in energy metabolism but have opposing effects.
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| 10. |
- Bohlooly-Yeganeh, Mohammad, 1966, et al.
(författare)
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Growth hormone overexpression in the central nervous system results in hyperphagia-induced obesity associated with insulin resistance and dyslipidemia.
- 2005
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Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 54:1, s. 51-62
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Tidskriftsartikel (refereegranskat)abstract
- It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intracerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect.
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