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In rabbits undergoing Escherichia coli meningitis, significant but late elevations in the excitatory amino acids aspartate and glutamate as well as in the inhibitory neurotransmitters γ-amino butyric acid and taurine were observed, which the authors assume – in contrast to the preceeding study – to be caused by cerebral ischaemia because of septic shock rather than the meningitis itself [ 29].
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The flux decay in this study was considered to be caused by gradual compression of the membrane which was confirmed by a compression test.
Mortality in this study was suggested to be caused by the toxicity of residual catalyst particles in the sample.
During this period, there were no other changes in pain management (e.g. change in immobilisation, regional blocks), so the effect observed in this pre-post study was likely to be caused by the intervention.
However, the long latencies observed in our study were likely to be caused by the EPSC propagation in the dendrites of postsynaptic neuron.
The differences in the lesion recurrence rates between the two pivotal studies are likely to be caused by the different way of counting recurrent lesions.
Inconsistencies among studies are again likely to be caused by variations in study methodology, particularly lack of detailed exposure assessment in some earlier studies.
Further studies elucidated the interaction to be caused by increased estradiol metabolism [ 39, 40].
Few were considered to be caused by study medication.
If the value was greater than 60%, sensitivity analysis was undertaken in an attempt to identify which studies were most likely to be causing the problem.
According to previous studies, this is caused by imperfectly melted and un-melted particles of raw materials during the flame spraying process [13, 14].
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