ObjectivesThis study compares rapid and traditional analyses of a UK health service evaluation dataset to explore differences in researcher time and consistency of outputs.DesignMixed methods study, quantitatively and qualitatively comparing qualitative methods.SettingData from a home birth service evaluation study in a hospital in the English National Health Service, which took place between October and December 2014. Two research teams independently analysed focus group and interview transcript data: one team used a thematic analysis approach using the framework method, and the second used rapid analysis.ParticipantsHome birth midwives (6), midwifery support workers (4), commissioners (4), managers (6), and community midwives (12) and a patient representative (1) participated in the original study.Primary outcome measuresTime taken to complete analysis in person hours; analysis findings and recommendations matched, partially matched or not matched across the two teams.ResultsRapid analysis data management took less time than thematic analysis (43 hours vs 116.5 hours). Rapid analysis took 100 hours, and thematic analysis took 126.5 hours in total, with interpretation and write up taking much longer in the rapid analysis (52 hours vs 8 hours). Rapid analysis findings overlapped with 79% of thematic analysis findings, and thematic analysis overlapped with 63% of the rapid analysis findings. Rapid analysis recommendations overlapped with 55% of those from the thematic analysis, and thematic analysis overlapped with 59% of the rapid analysis recommendations.ConclusionsRapid analysis delivered a modest time saving. Excessive time to interpret data in rapid analysis in this study may be due to differences between research teams. There was overlap in outputs between approaches, more in findings than recommendations. Rapid analysis may have the potential to deliver valid, timely findings while taking less time. We recommend further comparisons using additional data sets with more similar research teams.
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A rise in [Ca(2+)](i) provides the trigger for neurotransmitter release at neuronal boutons. We have used confocal microscopy and Ca(2+) sensitive dyes to directly measure the action potential-evoked [Ca(2+)](i) in the boutons of Schaffer collaterals. This reveals that the trial-by-trial amplitude of the evoked Ca(2+) transient is bimodally distributed. We demonstrate that "large" Ca(2+) transients occur when presynaptic NMDA receptors are activated following transmitter release. Presynaptic NMDA receptor activation proves critical in producing facilitation of transmission at theta frequencies. Because large Ca(2+) transients "report" transmitter release, their frequency on a trial-by-trial basis can be used to estimate the probability of release, p(r). We use this novel estimator to show that p(r) increases following the induction of long-term potentiation.
SK channels are small conductance Ca 2ϩ -activated K ϩ channels important for the control of neuronal excitability, the fine tuning of firing patterns, and the regulation of synaptic mechanisms. The classic SK channel pharmacology has largely focused on the peptide apamin, which acts extracellularly by a pore-blocking mechanism.
Shank3 is a structural protein found predominantly at the postsynaptic density. Mutations in the SHANK3 gene have been associated with risk for autism spectrum disorder (ASD). We generated induced pluripotent stem cells (iPSCs) from control individuals and from human donors with ASD carrying microdeletions of SHANK3. In addition, we used Zinc finger nucleases to generate isogenic SHANK3 knockout human embryonic stem (ES) cell lines. We differentiated pluripotent cells into either cortical or olfactory placodal neurons. We show that patient-derived placodal neurons make fewer synapses than control cells. Moreover, patient-derived cells display a developmental phenotype: young postmitotic neurons have smaller cell bodies, more extensively branched neurites, and reduced motility compared with controls. These phenotypes were mimicked by SHANK3-edited ES cells and rescued by transduction with a Shank3 expression construct. This developmental phenotype is not observed in the same iPSC lines differentiated into cortical neurons. Therefore, we suggest that SHANK3 has a critical role in neuronal morphogenesis in placodal neurons and that early defects are associated with ASD-associated mutations.
The behavior of the screw dislocation core in the presence of an external shear stress has been examined for the body-centered cubic and hexagonal close-packed phases of a model sodium lattice, using an effective ion–ion potential calculated from first principles. The Peierls stress for screw dislocations in the b.c.c. lattice at 0 °K is dependent on the orientation of the applied shear stress, and has a minimum value of 0.0105G, where G is the shear modulus, for slip in the twinning direction on {112} planes. The Peierls stress in the h.c.p. lattice is at least 25 times smaller. Dislocation movement in the model b.c.c. lattice takes place by unit translations on {110} planes, with the selection rule that no two consecutive translations can take place on the same slip plane.
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