Attribute elicitation

In our experience with FP, attribute elicitation is usually not a problan when working with experienced subjects or with product experts. Such subjects are indeed used to desoibing their sensations using descriptive terms. The only pitfall we met is when conducting an FP with panellists from a conventional profile panel heavily trained to describe the same category of products. Those subjects indeed tended to stick to the list of attributes they had learned before, and did not really adapt to the product set under study. 

The attribute elicitation issue may be considered differently when working with consumers. For instance, should one be interested in consumers spontaneous description, it would seem more pertinent to let the participants use their own terms without any suggestions. This may result in the elicitation of rather obvious attributes, although in past studies the vocabulary used by consumers was found to be rich and diverse (Veinand et al, 2011). On the contrary, providing a list may facilitate description (as in the Check-all-that-apply technique), but it may also bias consumers responses. However, these two options have not been formally compared yet, and ultimately the choice really has to be made with respect to the goals of the study. 

Should the experimenter decide to run the FP with a preliminary session, it must be made very clear to the panellists that the objective at this stage is to elicit discriminant attributes only. It would indeed be useless to generate an exhaustive list of attributes. In very few cases, it has indeed been observed that subjects who are used to attribute elicitation in QDA may misunderstand the task and generate a list of all potentially applicable attributes, which would be quite counterproductive. 

Second, in the FP procedure, the subjects are told to focus on the differences between the products. This implies that the subjects directly prioritize on major differences between the products and choose attributes accordingly. Dairou and Sieffermann (2002) have argued that this point certainly makes the attribute elicitation step more efficient. 

The term endocrine disrupter (ED) has tended to be used for those chemicals which act specifically at the level of the hormone receptor present in the target cells of various organs. Such chemicals may either mimic the action of the natural hormone (agonistic activity) or are sufficiently similar in molecular shape to the naturally produced hormone to interfere with the interaction between the hormone and receptor, thus blocking or impeding the activation of the receptor (antagonsitic activity). Such effects may occur at very low concentrations (as with the endogenous hormone), compared with the concentrations normally required to elicit the more traditional toxic effects attributed to chemicals. Recently,... 

When the partial agonist P occupies all the binding sites in order to produce its maximal response, pPR = 1. Hence, the stimulus (5P) attributable to P is simply eP Assuming that the same tissue response, whether elicited by A or by P, corresponds to the same value of 5, we can write ... 

Intestinal mechanical clearance thus consists of both reflex-mediated contractions (peristalsis) elicited by the stimulatory effect of luminal contents and of periods of spontaneous contractile activity (e.g. the migrating motor complex). During fasting about 50% of intestinal transit has been attributed to phase III of the migrating motor complex, the remaining mostly to the propulsive contractions and motor patterns during phase II [ 108]. Luminal flow can also occur in the absence of propagating contractions of the circular muscle layer, so far considered the motor event mainly responsible for flow in the small intestine. 

The role of C2 toxin in disease is not clear because all C. botulinum strains that produce C2 toxin also synthesize extremely potent neurotoxins, the effector molecules of botulism. When Simpson compared the pharmacological properties of C. botulinum neurotoxin type Cl with C2 toxin in detail, it became obvious that C2 toxin does not cause the flaccid paralysis symptoms attributed to classic botulism. However, isolated C2 toxin is a potent enterotoxin that proves lethal in various animals 2 pmol of C2 toxin readily kill mice, rats, guinea pigs, and chickens within 1 h after application. For mice, the LD50 (i.v.) of C2 toxin is less than 50 ftnol. Ohishi and Odagiri also reported that C2 toxin causes necrotic, hemorrhagic lesions in the intestinal wall, whereas Simpson reported that C2 toxin elicits hypotension as well as fluid accumulation in the lungs. ... 

Zwanzger et al. 2003). Administration of the neuropeptide ANP was effective in reducing the CCK-4-elicited panic reaction in patients with panic disorder and to a lesser extent in healthy controls. Moreover, ANP inhibited the CCK-4-induced rise of ACTH in both patients and controls, which may be attributed to a reduced hypothalamic CRH release (Jessop 1999 Wiedemann et al. 2001). Interestingly, ACTH release in response to CCK-4 was foimd to be blunted in patients when compared to healthy controls. This finding is possibly due to a chronic hypersecretion of CRH with a subsequent downregulation of CRH receptors in such patients (Wiedemann et al. 2001). 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

Both IgG and Csb were found to stimulate the respiratory burst separately and independently in one study but in another was active only in the presence of IgG. The divergent findings may be attributable to differing methods. In one study serum was mixed with agarose beads which fix complement with the binding of Csb- One set of beads was then heated at 50° for 30 min to remove 35 and the other was boiled in 2 M NaCl to remove IgG. The completeness of the removal of each component was verified by the loss of reactivity of the beads with a fluorescent monospecific antibody. Beads prepared in this way with either IgG or with Cjb attached elicited the formation of O by PMNs whereas the release of lysosomal contents occurred only with beads containing both IgG and Cab. The effects of the IgG-agarose were blocked by Ffab lj and those of Cjb were blocked by antiserum to C,. 

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