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Our case proves that an aggressive treatment should be undertaken and can be successful in CNS pseudallescheriasis.

Object The authors have previously reported that erlotinib, an EGFR tyrosine kinase inhibitor, exerts widely variable antiproliferative effects on 9 human glioblastoma multiforme (GBM) cell lines in vitro and in vivo. These effects were independent of EGFR baseline expression levels, raising the possibility that more complex genetic properties form the molecular basis of the erlotinib-sensitive and erlotinib-resistant GBM phenotypes. The aim of the present study was to determine candidate genes for mediating the cellular response of human GBMs to erlotinib. Methods Complementary RNA obtained in cell lines selected to represent the sensitive, somewhat responsive, and resistant phenotypes were hybridized to CodeLink Human Whole Genome Bioarrays. Results Expression analysis of 814 prospectively selected genes involved in major proliferation and apoptosis signaling pathways identified 19 genes whose expression significantly correlated with phenotype. Functional annotation analysis revealed that 2 genes (DUSP4 and STAT1) were significantly associated with sensitivity to erlotinib, and 10 genes (CACNG4, FGFR4, HSPA1B, HSPB1, NFATC1, NTRK1, RAC1, SMO, TCF7L1, and TGFB3) were associated with resistance to erlotinib. Moreover, 5 genes (BDNF, CARD6, FOSL1, HSPA9B, and MYC) involved in antiapoptotic pathways were unexpectedly found to be associated with sensitivity. Gene expressions were confirmed by quantitative polymerase chain reaction. Conclusions Based on an analysis of gene expressions in cell lines with sensitive, somewhat responsive, and resistant phenotypes, the authors propose candidate genes for GBM response to erlotinib. The 10 gene candidates for conferring GBM resistance to erlotinib may represent therapeutic targets for enhancing the efficacy of erlotinib against GBMs. Five additional genes warrant further investigation into their role as putative cotargets of erlotinib.

The use of the sitting position in neurosurgery is often associated with decreased arterial pressure (MAP) and stroke volume index (SVI). A shift in blood from the intra- to the extrathoracic compartment may be responsible for this cardiovascular response. However, little is known of the amount of shift in blood volume after transfer from the supine to the sitting position. Therefore, we measured simultaneously changes in intrathoracic blood volume (ITBV) caused by a change in body position in anaesthetized patients. Measurements of cardiac index (CI), ITBV, pulmonary (PBV) and total circulating (TBVcirc) blood volumes were performed in the supine and sitting position. CI, ITBV, PBV and TBVcirc were measured using a thermodye dilution technique. Fluid input was restricted to 14 ml kg-1 before induction of anaesthesia. Change in body position caused a significant decrease in ITBV and was accompanied by a significant decrease in CI, SVI and MAP. Changes in ITBV correlated (r = 0.78) with changes in SVI. Thus a change in blood volume distribution between the intra- and extrathoracic compartment occurred after a change from the supine to the sitting position. Indicator dilution enables quantification of this shift and may be helpful in guiding fluid therapy in selected patients.