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Deze studie laat zien dat een abrupte kleurverandering gepresenteerd tegen een isoluminante achtergrond geen pop-out geeft.

It has been generally assumed that fat is detected by its flavour and by its lubrication of the oral mucosa. A recent study reported a correlation of -.99 between perceived temperature of a product and its fat content. This was significantly higher than correlations of sensory scores for fat flavour, mouthfeel, and afterfeel. This suggested a third detection mechanism; fat may be detected via its effect on the thermal conductivity of the food. In 3 studies, thermal sensitivity in humans was investigated to verify whether oral thermal receptors are sufficiently rapid and accurate to play a role in the perception of fats. The thermal sensitivity of the lips and oral mucosa of the anterior and middle one-third of the tongue were assessed using a Peltier device. Subjects detected 0.5 Hz fluctuations in temperature of 0.08°C on the lower lip, 0.26°C and 1.36°C at the tip and dorsum of the tongue, demonstrating that the lips are sufficiently sensitive to detect small differences in temperature. In two further experiments subjects ingested custards and mayonnaises and then spat out samples after 5, 10, or 20 sec. The temperature of the food and oral mucosa was measured before and after spitting and the rates of heating were calculated. Results suggest assessment of thermal conductivity of food may be used to assess fat content. © Perceptual and Motor Skills 2007. Chemicals / CAS: Dietary Fats

Poisoning with the potent nerve agent soman produces a cascade of central nervous system (CNS) effects characterized by severe convulsions and eventually death. In animals that survive a soman intoxication, lesions in the amygdala, piriform cortex, hippocampus and thalamus can be observed. In order to examine the mechanisms involved in the effects of soman and to evaluate possible curative interventions, a series of behavioural, electrophysiological and neuropathological experiments were carried out in the guinea pig using the NMDA antagonist N-[1-(2-thienyl)cyclohexyl] piperidine (TCP) in conjunction with atropine and pyridostigmine. The NMDA antagonist TCP appeared to be very effective in the treatment of casualties who suffered from soman-induced seizures for 30 min: (i)Seizures were arrested within minutes after the TCP injection, confirmed by quantitative electroencephalogram (EEG), after fast Fourier analysis. Three hours after TCP the quantitative EEGs were completely normal in all frequency bands and remained normal during the entire 3-week intoxication period. The power shift to the lower (delta) frequency bands, indicative for neuropathology and found in control animals intoxicated only by soman, was not observed in the soman-TCP group. (ii)The gross neuropathology found in soman control animals within 48 h after soman was prevented in soman-TCP animals and was still absent in 3-week survivors. Instead, ultrastructural changes were observed, indicative of defense mechanisms of the cell against toxic circumstances. (iii)Twenty-four hours after soman, soman-TCP animals were able to perform in the shuttle box and Morris water maze. The beneficial effects of TCP on the performance in these tests during the 3-week intoxication period were very impressive, notwithstanding (minor) deficits in memory and learning. (iv)The increase in excitability after TCP was confirmed by an increase in the acoustic startle response. Taken together, these results confirmed the involvement of NMDA receptors in the maintenance of soman-induced seizures and the development of brain damage. They underline the current hypothesis that cholinergic mechanisms are responsible for eliciting seizure activity after soman and that, most likely, the subsequent recruitment of other excitatory neurotransmitters and loss of inhibitory control are responsible for the maintenance of seizures and the development of subsequent brain damage. Copyright 2001 John Wiley & Sons, Ltd.Chemicals/CAS: 1-(1-(2-thienyl)cyclohexyl)piperidine, 21500-98-1; Atropine, 51-55-8; Chemical Warfare Agents; Cholinesterase Inhibitors; Muscarinic Antagonists; Neuroprotective Agents; Phencyclidine, 77-10-1; Pyridostigmine Bromide, 101-26-8; Receptors, N-Methyl-D-Aspartate; Soman, 96-64-0

The toxicity of inhalatory exposure to organic solvents may not only be related to the total external dose, but also to the pattern of exposure. In this study physiologically based toxicokinetic (PBTK) modelling has been used to study the impact of the exposure scenario on the toxicokinetics and the behavioural effects of the model solvent toluene in rats. After construction of the model with parameters from literature, toxicokinetic data were collected from rats exposed to either a constant concentration or fluctuating concentrations at total external dose levels of 20 000 and 10 000 ppm×h for model validation. At the same exposure conditions the effects on learned performance were evaluated in separate groups of rats using a visual discrimination task. In general, the PBTK model provided reliable predictions of the toxicokinetics of toluene at different exposure scenarios, but it also tended to underestimate the blood and brain concentrations in the descending parts of the tissue concentration-time curves. At these high dose levels the differences in toxicokinetics between the constant and the fluctuating exposure groups were relatively small. The visual discrimination experiments demonstrated a slowing of response speed and disinhibition of responding in all toluene-exposed groups. The results suggest that the brain concentration of toluene is one of the major determinants of its effect on disinhibition of responding. © 2002 Elsevier Science Ireland Ltd. All rights reserved.