Background: Although Aspergillus fumigatus is an important human fungal pathogen there are few expression systems available to study the contribution of specific genes to the growth and virulence of this opportunistic mould. Regulatable promoter systems based upon prokaryotic regulatory elements in the E. coli tetracycline-resistance operon have been successfully used to manipulate gene expression in several organisms, including mice, flies, plants, and yeast. However, the system has not yet been adapted for Aspergillus spp.

In this study, we sought to examine the effect of experimentally-induced somatic pain on memory. Subjects heard a series of words and made categorization decisions in two different conditions. One condition included painful shocks administered just after presentation of some of the words; the other condition involved no shocks. For the condition that included painful stimulations, every other word was followed by a shock, and subjects were informed to expect this pattern. Word lists were repeated three times within each condition in randomized order, with different category judgments but consistent pain-word pairings. After a brief delay, recognition memory was assessed. Non-pain words from the pain condition were less strongly encoded than non-pain words from the completely pain-free condition. Recognition of pain-paired words was not significantly different than either subgroup of non-pain words. An important accompanying finding is that response times to repeated experimental items were slower for non-pain words from the pain condition, compared to non-pain words from the completely pain-free condition. This demonstrates that the effect of pain on memory may generalize to non-pain items experienced in the same experimental context.

Respiratory motion and capnometry monitoring were performed during blood oxygen level dependent (BOLD) functional magnetic resonance imaging (FMRI) of the brain while a series of paced hyperventilation tasks were performed that caused significant hypocapnia. Respiration volume per time (RVT) and end-tidal carbon dioxide (ETCO2) were determined and compared for their ability to explain BOLD contrast changes in the data. A 35% decrease in ETCO2 was observed along with corresponding changes in RVT. A best-fit ETCO2 response function, with an average initial peak delay time of 12 s, was empirically determined. ETCO2 data convolved with this response function was more strongly and prevalently correlated to BOLD signal changes than RVT data convolved with the corresponding respiration response function. The results suggest that ETCO2 better models BOLD signal fluctuations in FMRI experiments with significant transient hypocapnia. This is due to hysteresis in the ETCO2 response when moving from hypocapnia to normocapnia, compared to moving from normocapnia to hypocapnia.

The temporal dynamics of the blood oxygen level dependent (BOLD) signal, especially for painful stimulations, is not completely understood. In this study, the BOLD signal response to a long painful electrical stimulation (a continuous painful stimulation of 2 minutes) is directly compared to that of a short painful stimulation (four 30-s periods of painful stimulation interleaved with 30-s rest) in an effort to further probe the relationship between the temporal dynamics of the BOLD signal during constant intensity pain stimulation. Time course analysis showed that both stimulation protocols produced three similarly timed peaks in both data sets, suggesting an early and delayed BOLD response to painful stimulation initiation, and a response related to stimulus termination. Despite the continuous stimulation, the BOLD signal returned to baseline in the two-minute task. Even with this signal discrepancy, however, the activation maps of the two pain tasks differed only slightly, suggesting that the bulk of the activation is determined by the sharp rise in BOLD signal with stimulus onset. These findings imply that the BOLD signal response time course is not directly reflective of pain perception.