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- Fornander, Liselott, 1981-
(författare)
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How we talk : aspects of communication and team cognition of trauma resuscitation teams
- 2024
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- A trauma team consists of professionals assembling in an ad hoc manner to resuscitate a patient with life-threatening injuries. In such a team, how the team manages to use non-technical skills, such as communication is important to achieve task management and decision making. Communication is practised in simulations, and the simulation environment has also been used in research to understand teamwork processes. This thesis is based on video observations of trauma teams working in real life (IRL) and in situ simulations of trauma resuscitations. The aim was to assess the creation of team cognition IRL and in simulation, to analyse verbal communication in the teams and the effects of real-time communication on team structure. In Study I, a grounded theory analysis was undertaken to understand how verbal and non-verbal interactions create team cognition. The analysis resulted in a theory pointing to “split vision” as a team’s ability to alter process modes between team positioning and sensitivity to the patient that was dependent on patient and situational values absorbed from team members’ implicit actions. In Study II, the verbal response modes taxonomy was applied to analyse both the grammatical and pragmatic meaning of verbal interactions that were compared between team roles. In the six most communicative team roles in the context of IRL trauma teamwork, pure mode communication dominated the way of delivering messages. In Study III, the structures of four IRL and four simulated trauma teams were analysed using a social network analysis of real-time communication. Overall, the teams were highly centralised, with the examining physician functioning as an information hub. In Study IV, communication from the same teams was categorised according to information and task management, as well as different coordination behaviours. We compared the IRL and simulation domains based on the proportions of utterances of each category/code, and found that “Give information after request” and closed-loop communication were more prevalent in simulation. Observing real-time communications using different methodologies gave a perspective on the conditions and possibilities for adaptation in terms of work prescriptions and team training, such as room for more communication and possible congestions of nodes in terms of occupancy and tacit communications and working modes thus far unnoticed by us and unreported. Such understanding complements established knowledge about coordination behaviours and interactive team cognition and should be taken into consideration in the practise and training of trauma teams.
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| 3. |
- Björnström, Karin, 1971-, et al.
(författare)
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A tyrosine kinase regulates propofol-induced modulation of the beta-subunit of the GABA(A) receptor and release of intracellular calcium in cortical rat neurones
- 2002
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 175:3, s. 227-235
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Tidskriftsartikel (refereegranskat)abstract
- Propofol, an intravenous anaesthetic, has been shown to interact with the beta -subunit of the gamma -amino butyric acid(A) (GABA(A) ) receptor and also to cause changes in [Ca2+ ](i) . The GABA(A) receptor, a suggested target for anaesthetics, is known to be regulated by kinases. We have investigated if tyrosine kinase is involved in the intracellular signal system used by propofol to cause anaesthesia. We used primary cell cultured neurones from newborn rats, pre-incubated with or without a tyrosine kinase inhibitor before propofol stimulation. The effect of propofol on tyrosine phosphorylation and changes in [Ca2+ ](i) were investigated. Propofol (3 mu g mL(-1) , 16.8 mu M) increased intracellular calcium levels by 122 +/- 34% (mean +/- SEM) when applied to neurones in calcium free medium. This rise in [Ca2+ ](i) was lowered by 68% when the cells were pre-incubated with the tyrosine kinase inhibitor herbimycin A before exposure to propofol (P < 0.05). Propofol caused an increase (33 +/- 10%) in tyrosine phosphorylation, with maximum at 120 s, of the beta -subunit of the GABA(A) -receptor. This tyrosine phosphorylation was decreased after pre-treatment with herbimycin A (44 +/- 7%, P < 0.05), and was not affected by the absence of exogenous calcium in the medium. Tyrosine kinase participates in the propofol signalling system by inducing the release of calcium from intracellular stores and by modulating the beta -subunit of the GABA(A) -receptor.
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| 4. |
- Björnström, Karin, 1971-, et al.
(författare)
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Characterisation of the signal transduction cascade caused by propofol in rat neurons : From the GABAA receptor to the cytoskeleton
- 2008
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Ingår i: Journal of Physiology and Pharmacology. - 0867-5910 .- 1899-1505. ; 59:3, s. 617-632
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Tidskriftsartikel (refereegranskat)abstract
- The anaesthetic propofol interacts with the GABAA receptor, but its cellular signalling pathways are not fully understood. Propofol causes reorganisation of the actin cytoskeleton into ring structures in neurons. Is this reorganisation a specific effect of propofol as apposed to GABA, and which cellular pathways are involved? We used fluorescence-marked actin in cultured rat neurons to evaluate the percentage of actin rings caused by propofol or GABA in combination with rho, rho kinase (ROK), PI3-kinase or tyrosine kinase inhibitors, with or without the presence of extracellular calcium. Confocal microscopy was performed on propofol-stimulated cells and changes in actin between cellular compartments were studied with Western blot. Propofol (3 μg·ml-1), but not GABA (5 μM), caused transcellular actin ring formation, that was dependent on influx of extracellular calcium and blocked by rho, ROK, PI3-kinase or tyrosine kinase inhibitors. Propofol uses rho/ROK to translocate actin from the cytoskeleton to the membrane and its actin ring formation is dependent on an interaction site close to the GABA site on the GABAA receptor. GABA does not cause actin rings, implying that this is a specific effect of propofol.
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| 5. |
- Björnström, Karin, 1971-, et al.
(författare)
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The difference between sleep and anaesthesia is in the intracellular signal : propofol and GABA use different subtypes of the GABAA receptor β subunit and vary in their interaction with actin
- 2003
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 47:2, s. 157-164
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Tidskriftsartikel (refereegranskat)abstract
- Background: Propofol is known to interact with the γ-aminobutyric acidA (GABAA) receptor, however, activating the receptor alone is not sufficient for producing anaesthesia.Methods: To compare propofol and GABA, their interaction with the GABAA receptor β subunit and actin were studied in three cellular fractions of cultured rat neurons using Western blot technique.Results: Propofol tyrosine phosphorylated the GABAA receptor β2 (MW 54 and 56 kDa) and β3 (MW 57 kDa) subtypes. The increase was shown in both the cytoskeleton (β2(54) and β2(56) subtypes) and the cell membrane (β2(54) and β3 subtypes). Concurrently the 56 kDa β2 subtype was reduced in the cytosol. Propofol, but not GABA, also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. Without extracellular calcium available, the amount of actin decreased in the cytoskeleton, but tyrosine phosphorylation was unchanged. GABA caused increased tyrosine phosphorylation of β2(56) and β3 subtypes in the membrane and both β2 subtypes in the cytoskeleton but no cytosolic tyrosine phosphorylation.Conclusion: The difference between propofol and GABA at the GABAA receptor was shown to take place in the membrane, where the β2(54) was increased by propofol and instead the β2(56) subtype was increased by GABA. Only propofol also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. This interaction between the GABAA receptor and actin might explain the difference between anaesthesia and physiological neuronal inhibition.
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- Björnström Karlsson, Karin, 1971-
(författare)
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Cellular mechanisms of anaesthetic agents
- 2003
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Anaesthesia is given to approximate 5% of the Swedish population annually, with the great advantage of painless surgery, but it also has side effects such as depression of blood pressure that might give a heart infarction. Exactly how anaesthetic agents cause anaesthesia is poorly known. Most anaesthetics have been shown to interact with the GABAA receptor, whose endogenous ligand GABA causes down-regulation of the brain and sleep. To further explore the cellular signal system used by anaesthetics this study was performed.First, two different malignant cell lines, PC-12 and SH-SY5Y, were tested, to evaluate if they could replace animal cells; however, they did not respond with increased intracellular calcium [Ca2+]i upon stimulation with propofol, as the normal rat neurons do. This is probably due to differences in the intracellular signaling systems in these malignant cells. Therefore, the studies in this thesis were performed on rat neurons.Propofol, an intravenous anaesthetic, was shown to cause a bicucullin insensitive increase in [Ca2+]i, where the release from intracellular stores was dependent on a tyrosine kinase. Sevoflurane, a volatile anaesthetic, also caused an ilrunediate increase in [Ca2+]i, but not nitrous oxide. Increased [Ca2+], is supposed to augment the influx of chloride ions through the GABAA receptor, hence hyperpolarising the neuron, and thereby make it anaesthetised.Tyrosine phosphorylation of the GABAA receptor is necessary for its function. Propofol tyrosine phosphorylates another ß2 subunit in the membrane then GABA. Propofol, but not GABA, also caused a tyrosine phosphorylation of actin in both the cytoskeletal and cell membrane fraction. Together these changes might explain the difference between sleep and anaesthesia. Isoflurane, sevoflurane and nitrous oxide all tyrosine phosphmylate a protein, suggested to be the GABAA receptor ß subunit, in different cellular compartments. This might explain their different clinical effects.Propofol and sevoflurane, but not GABA, causes actin rings to be formed in the cell, and for propofol the signal goes via rhoA and rho kinase, that also are involved in the translocation of actin to the cellular membrane. An unl~own 160 kDa protein is tyrosine phosphorylated by propofol, is part of the rho signalling pathway and is regulated by rho, This unknown protein might be involved in the actin reorganisation.
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