44 research outputs found
Atmospheric oxygenation caused by a change in volcanic degassing pressure
International audienceThe Precambrian history of our planet is marked by two major events: a pulse of continental crust formation at the end of the Archaean eon and a weak oxygenation of the atmosphere (the Great Oxidation Event) that followed, at 2.45 billion years ago. This oxygenation has been linked to the emergence of oxygenic cyanobacteria1,2 and to changes in the compositions of volcanic gases3,4, but not to the composition of erupting lavas--geochemical constraints indicate that the oxidation state of basalts and their mantle sources has remained constant since 3.5 billion years ago5,6. Here we propose that a decrease in the average pressure of volcanic degassing changed the oxidation state of sulphur in volcanic gases, initiating themodern biogeochemical sulphur cycle and triggering atmospheric oxygenation. Using thermodynamic calculations simulating gas-melt equilibria in erupting magmas, we suggest that mostly submarine Archaean volcanoes produced gases with SO2/H2S,1 and low sulphur content. Emergence of the continents due to a global decrease in sea level and growth of the continental crust in the late Archaean then led to widespread subaerial volcanism, which in turn yielded gases much richer in sulphur and dominated bySO2. Dissolution of sulphur in sea water and the onset of sulphate reduction processes could then oxidize the atmosphere
Conditioned task-set competition:Neural mechanisms of emotional interference in depression
Depression has been associated with increased response times at the incongruent, neutral, and negative-word trials of the classical and emotional Stroop tasks (Epp et al., 2012). Response time slow-down effects at incongruent and negative-word trials of the Stroop tasks were reported to correlate with depressive severity, indicating strong relevance of the effects to the symptomatology. The current study proposes a novel integrative computational model of neural mechanisms of both the classical and the emotional Stroop effects, drawing on the previous prominent theoretical explanations of performance at the classical Stroop task (Cohen et al., 1990; Herd et al., 2006), and in addition suggesting that negative emotional words represent conditioned stimuli for future negative outcomes. The model is shown to explain the classical Stroop effect and the slow (between-trial) emotional Stroop effect with biologically-plausible mechanisms, providing an advantage over the previous theoretical accounts (Matthews and Harley, 1996; Wyble et al., 2008). Simulation results suggested a candidate mechanism responsible for the pattern of depressive performance at the classical and the emotional Stroop tasks. Hyperactivity of the amygdala, together with increased inhibitory influence of the amygdala over dopaminergic neurotransmission, could be at the origin of the performance deficits
Does reductive metabolism predict response to tirapazamine (SR 4233) in human non-small-cell lung cancer cell lines?
The bioreductive drug tirapazamine (TPZ, SR 4233, WIN 59075) is a lead compound in a series of potent cytotoxins that selectively kill hypoxic rodent and human solid tumour cells in vitro and in vivo. Phases II and III trials have demonstrated its efficacy in combination with both fractionated radiotherapy and some chemotherapy. We have evaluated the generality of an enzyme-directed approach to TPZ toxicity by examining the importance of the one-electron reducing enzyme NADPH:cytochrome P450 reductase (P450R) in the metabolism and toxicity of this lead prodrug in a panel of seven human non-small-cell lung cancer cell lines. We relate our findings on TPZ sensitivity in these lung lines with our previously published results on TPZ sensitivity in six human breast cancer cell lines (Patterson et al (1995) Br J Cancer 72: 1144–1150) and with the sensitivity of all these cell types to eight unrelated cancer chemotherapeutic agents with diverse modes of action. Our results demonstrate that P450R plays a significant role in the activation of TPZ in this panel of lung lines, which is consistent with previous observations in a panel of breast cancer cell lines (Patterson et al (1995) Br J Cancer 72: 1144–1150; Patterson et al (1997) Br J Cancer 76: 1338–1347). However, in the lung lines it is likely that it is the inherent ability of these cells to respond to multiple forms of DNA damage, including that arising from P450R-dependent TPZ metabolism, that underlies the ultimate expression of toxicity. © 1999 Cancer Research Campaig
Characterisation of the Wildlife Reservoir Community for Human and Animal Trypanosomiasis in the Luangwa Valley, Zambia
Animal and human trypanosomiasis are constraints to both animal and human health in Sub-Saharan Africa, but there is little recent evidence as to how these parasites circulate in natural hosts in natural ecosystems. A cross-sectional survey of trypanosome prevalence in 418 wildlife hosts was conducted in the Luangwa Valley, Zambia, from 2005 to 2007. The overall prevalence in all species was 13.9%. Infection was significantly more likely to be detected in waterbuck, lion, greater kudu and bushbuck, with a clear pattern apparent of the most important hosts for each trypanosome species. Human infective Trypanosoma brucei rhodesiense parasites were identified for the first time in African buffalo and T. brucei s.l. in leopard. Variation in infection is demonstrated at species level rather than at family or sub-family level. A number of significant risk factors are shown to interact to influence infection rates in wildlife including taxonomy, habitat and blood meal preference. Trypanosoma parasites circulate within a wide and diverse host community in this bio-diverse ecosystem. Consistent land use patterns over the last century have resulted in epidemiological stability, but this may be threatened by the recent influx of people and domesticated livestock into the mid-Luangwa Valley
Weed or wheel! FMRI, behavioural, and toxicological investigations of how cannabis smoking affects skills necessary for driving.
Marijuana is the most widely used illicit drug, however its effects on cognitive functions underling safe driving remain mostly unexplored. Our goal was to evaluate the impact of cannabis on the driving ability of occasional smokers, by investigating changes in the brain network involved in a tracking task. The subject characteristics, the percentage of Δ(9)-Tetrahydrocannabinol in the joint, and the inhaled dose were in accordance with real-life conditions. Thirty-one male volunteers were enrolled in this study that includes clinical and toxicological aspects together with functional magnetic resonance imaging of the brain and measurements of psychomotor skills. The fMRI paradigm was based on a visuo-motor tracking task, alternating active tracking blocks with passive tracking viewing and rest condition. We show that cannabis smoking, even at low Δ(9)-Tetrahydrocannabinol blood concentrations, decreases psychomotor skills and alters the activity of the brain networks involved in cognition. The relative decrease of Blood Oxygen Level Dependent response (BOLD) after cannabis smoking in the anterior insula, dorsomedial thalamus, and striatum compared to placebo smoking suggests an alteration of the network involved in saliency detection. In addition, the decrease of BOLD response in the right superior parietal cortex and in the dorsolateral prefrontal cortex indicates the involvement of the Control Executive network known to operate once the saliencies are identified. Furthermore, cannabis increases activity in the rostral anterior cingulate cortex and ventromedial prefrontal cortices, suggesting an increase in self-oriented mental activity. Subjects are more attracted by intrapersonal stimuli ("self") and fail to attend to task performance, leading to an insufficient allocation of task-oriented resources and to sub-optimal performance. These effects correlate with the subjective feeling of confusion rather than with the blood level of Δ(9)-Tetrahydrocannabinol. These findings bolster the zero-tolerance policy adopted in several countries that prohibits the presence of any amount of drugs in blood while driving
