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1.  SO2 protects the amino nitrogen metabolism of Saccharomyces cerevisiae under thermal stress 
Microbial biotechnology  2012;5(5):654-662.
Thermal stress conditions during alcoholic fermentation modify yeasts' plasma membrane since they become more hyperfluid, which results in a loss of bilayer integrity. In this study, the influence of elevated temperatures on nitrogen metabolism of a Saccharomyces cerevisiae strain was studied, as well as the effect of different concentrations of SO2 on nitrogen metabolism under thermal stress conditions. The results obtained revealed that amino nitrogen consumption was lower in the fermentation sample subjected to thermal stress than in the control, and differences in amino acid consumption preferences were also detected, especially at the beginning of the fermentation. Under thermal stress conditions, among the three doses of SO2 studied (0, 35, 70 mg l−1 SO2), the highest dose was observed to favour amino acid utilization during the fermentative process, whereas sugar consumption presented higher rates at medium doses.
PMCID: PMC3815877  PMID: 22452834
2.  The Rover Environmental Monitoring Station Ground Temperature Sensor: A Pyrometer for Measuring Ground Temperature on Mars 
Sensors (Basel, Switzerland)  2010;10(10):9211-9231.
We describe the parameters that drive the design and modeling of the Rover Environmental Monitoring Station (REMS) Ground Temperature Sensor (GTS), an instrument aboard NASA’s Mars Science Laboratory, and report preliminary test results. REMS GTS is a lightweight, low-power, and low cost pyrometer for measuring the Martian surface kinematic temperature. The sensor’s main feature is its innovative design, based on a simple mechanical structure with no moving parts. It includes an in-flight calibration system that permits sensor recalibration when sensor sensitivity has been degraded by deposition of dust over the optics. This paper provides the first results of a GTS engineering model working in a Martian-like, extreme environment.
PMCID: PMC3230958  PMID: 22163405
IR ground temperature sensor; sensor thermal model; spacecraft instrumentation; in-flight calibration
3.  The pharmacology of the acute hyperthermic response that follows administration of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy') to rats 
British Journal of Pharmacology  2002;135(1):170-180.
The pharmacology of the acute hyperthermia that follows 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy') administration to rats has been investigated.MDMA (12.5 mg kg−1 i.p.) produced acute hyperthermia (measured rectally). The tail skin temperature did not increase, suggesting that MDMA may impair heat dissipation.Pretreatment with the 5-HT1/2 antagonist methysergide (10 mg kg−1), the 5-HT2A antagonist MDL 100,907 (0.1 mg kg−1) or the 5-HT2C antagonist SB 242084 (3 mg kg−1) failed to alter the hyperthermia. The 5-HT2 antagonist ritanserin (1 mg kg−1) was without effect, but MDL 11,939 (5 mg kg−1) blocked the hyperthermia, possibly because of activity at non-serotonergic receptors.The 5-HT uptake inhibitor zimeldine (10 mg kg−1) had no effect on MDMA-induced hyperthermia. The uptake inhibitor fluoxetine (10 mg kg−1) markedly attenuated the MDMA-induced increase in hippocampal extracellular 5-HT, also without altering hyperthermia.The dopamine D2 antagonist remoxipride (10 mg kg−1) did not alter MDMA-induced hyperthermia, but the D1 antagonist SCH 23390 (0.3 – 2.0 mg kg−1) dose-dependently antagonized it.The dopamine uptake inhibitor GBR 12909 (10 mg kg−1) did not alter the hyperthermic response and microdialysis demonstrated that it did not inhibit MDMA-induced striatal dopamine release.These results demonstrate that in vivo MDMA-induced 5-HT release is inhibited by 5-HT uptake inhibitors, but MDMA-induced dopamine release may not be altered by a dopamine uptake inhibitor.It is suggested that MDMA-induced hyperthermia results not from MDMA-induced 5-HT release, but rather from the increased release of dopamine that acts at D1 receptors. This has implications for the clinical treatment of MDMA-induced hyperthermia.
PMCID: PMC1573106  PMID: 11786492
3,4-methylenedioxymethamphetamine; ecstasy; hyperthermia; dopamine; 5-hydroxytryptamine; 5-HT antagonists; dopamine antagonists; GBR 12909; fluoxetine
4.  A study of the mechanisms involved in the neurotoxic action of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy') on dopamine neurones in mouse brain 
British Journal of Pharmacology  2001;134(8):1711-1723.
Administration of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy') to mice produces acute hyperthermia and long-term degeneration of striatal dopamine nerve terminals. Attenuation of the hyperthermia decreases the neurodegeneration. We have investigated the mechanisms involved in producing the neurotoxic loss of striatal dopamine.MDMA produced a dose-dependent loss in striatal dopamine concentration 7 days later with 3 doses of 25 mg kg−1 (3 h apart) producing a 70% loss.Pretreatment 30 min before each MDMA dose with either of the N-methyl-D-aspartate antagonists AR-R15896AR (20, 5, 5 mg kg−1) or MK-801 (0.5 mg kg−1×3) failed to provide neuroprotection.Pretreatment with clomethiazole (50 mg kg−1×3) was similarly ineffective in protecting against MDMA-induced dopamine loss.The free radical trapping compound PBN (150 mg kg−1×3) was neuroprotective, but it proved impossible to separate neuroprotection from a hypothermic effect on body temperature.Pretreatment with the nitric oxide synthase (NOS) inhibitor 7-NI (50 mg kg−1×3) produced neuroprotection, but also significant hypothermia. Two other NOS inhibitors, S-methyl-L-thiocitrulline (10 mg kg−1×3) and AR-R17477AR (5 mg kg−1×3), provided significant neuroprotection and had little effect on MDMA-induced hyperthermia.MDMA (20 mg kg−1) increased 2,3-dihydroxybenzoic acid formation from salicylic acid perfused through a microdialysis tube implanted in the striatum, indicating increased free radical formation. This increase was prevented by AR-R17477AR administration. Since AR-R17477AR was also found to have no radical trapping activity this result suggests that MDMA-induced neurotoxicity results from MDMA or dopamine metabolites producing radicals that combine with NO to form tissue-damaging peroxynitrites.
PMCID: PMC1572911  PMID: 11739248
3,4-methylenedioxymethamphetamine; MDMA; ecstasy; NMDA antagonists; nitric oxide synthase inhibitors; clomethiazole; PBN; free radicals; dopamine; neuroprotection

Results 1-4 (4)