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Gas sensor investigation based on a catalytically activated thin-film thermopile for H2O2 detection
(2010)
Short term effects of magnetic resonance imaging on excitability of the motor cortex at 1.5T and 7T
(2010)
Rationale and Objectives
The increasing spread of high-field and ultra-high-field magnetic resonance imaging (MRI) scanners has encouraged new discussion of the safety aspects of MRI. Few studies have been published on possible cognitive effects of MRI examinations. The aim of this study was to examine whether changes are measurable after MRI examinations at 1.5 and 7 T by means of transcranial magnetic stimulation (TMS).
Materials and Methods
TMS was performed in 12 healthy, right-handed male volunteers. First the individual motor threshold was specified, and then the cortical silent period (SP) was measured. Subsequently, the volunteers were exposed to the 1.5-T MRI scanner for 63 minutes using standard sequences. The MRI examination was immediately followed by another TMS session. Fifteen minutes later, TMS was repeated. Four weeks later, the complete setting was repeated using a 7-T scanner. Control conditions included lying in the 1.5-T scanner for 63 minutes without scanning and lying in a separate room for 63 minutes. TMS was performed in the same way in each case. For statistical analysis, Wilcoxon's rank test was performed.
Results
Immediately after MRI exposure, the SP was highly significantly prolonged in all 12 subjects at 1.5 and 7 T. The motor threshold was significantly increased. Fifteen minutes after the examination, the measured value tended toward normal again. Control conditions revealed no significant differences.
Conclusion
MRI examinations lead to a transient and highly significant alteration in cortical excitability. This effect does not seem to depend on the strength of the static magnetic field.
Purpose
To assess potential cognitive deficits under the influence of static magnetic fields at various field strengths some studies already exist. These studies were not focused on attention as the most vulnerable cognitive function. Additionally, mostly no magnetic resonance imaging (MRI) sequences were performed.
Materials and Methods
In all, 25 right-handed men were enrolled in this study. All subjects underwent one MRI examination of 63 minutes at 1.5 T and one at 7 T within an interval of 10 to 30 days. The order of the examinations was randomized. Subjects were referred to six standardized neuropsychological tests strictly focused on attention immediately before and after each MRI examination. Differences in neuropsychological variables between the timepoints before and after each MRI examination were assessed and P-values were calculated
Results
Only six subtests revealed significant differences between pre- and post-MRI. In these tests the subjects achieved better results in post-MRI testing than in pre-MRI testing (P = 0.013–0.032). The other tests revealed no significant results.
Conclusion
The improvement in post-MRI testing is only explicable as a result of learning effects. MRI examinations, even in ultrahigh-field scanners, do not seem to have any persisting influence on the attention networks of human cognition immediately after exposure.
Dexamethasone (DEX) is a potent and widely used anti-inflammatory and immunosuppressant glucocorticoid. It can bind and activate the pregnane X receptor (PXR), which plays a critical role as xenobiotic sensor in mammals to induce the expression of many enzymes, including cytochromes P450 in the CYP3A family. This induction results in its own metabolism. We have used a series of transgenic mouse lines, including a novel, improved humanized PXR line, to compare the induction profile of PXR-regulated drug-metabolizing enzymes after DEX administration, as well as looking at hepatic responses to rifampicin (RIF). The new humanized PXR model has uncovered further intriguing differences between the human and mouse receptors in that RIF only induced Cyp2b10 in the new humanized model. DEX was found to be a much more potent inducer of Cyp3a proteins in wild-type mice than in mice humanized for PXR. To assess whether PXR is involved in the detoxification of DEX in the liver, we analyzed the consequences of high doses of the glucocorticoid on hepatotoxicity on different PXR genetic backgrounds. We also studied these effects in an additional mouse model in which functional mouse Cyp3a genes have been deleted. These strains exhibited different sensitivities to DEX, indicating a protective role of the PXR and CYP3A proteins against the hepatotoxicity of this compound.