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Sensory Implications

As with other flavor and odor-active compounds in wine, detection and interpretation (either positive or negative) depend on the matrix in which those components are present. In the case of acetic acid, aroma thresholds (in wine) have been reported to be as low as 100-125 mg/L (Riesen, 1992). The concentration at which the acid is regarded as detrimental is considerably higher, ranging from 700 mg/L (Zoecklein et al., 1995) to 1200-1300 mg/L reported by Margalith (1981). The latter two levels are at, or exceed, legal maxima as established for table wines by both OlV and BATF (see Table 2-3). [Pg.59]

Aside from its intrinsic sensory properties, acetic acid may modify the perception of other wine constituents. For example, fixed acidity and tannins may be intensified. Conversely, higher levels of sugar and alcohol tend to mask the presence of potentially objectionable concentrations of the acid (Zoecklein et al., 1995). [Pg.59]


Aside from potential sensory implications, acetic acid and associated products of LAB metabolism represent potent inhibitors to fermentatively growing Saccharomyces, delaying the onset of fermentation and potentially causing fermentation to stick (see previous discussion of Microbial Antagonism). At pH >3.5, bacterial carbohydrate metabolism (Peynaud and Domercq, 1968) or MLF (Giannakopoulis et al., 1984 Zeeman et al., 1982) yielded higher concentrations of acetic acid than parallel lots at a lower pH. [Pg.29]

An additional and widespread neuroactive (transmitter-like) compound is nitric oxide (NO). This gaseous secretion is a product of the action of the enzyme NO-synthase on arginine. It is implicated in at least two roles within the non-sensory tissues of the organ, and at particular synapses in the AOB. One nitric oxidergic effect is initiated by the nerve fibres supplying the smooth muscle component of the vasomotor tissues. The other effect is the expected action of NO on the output... [Pg.100]

Henkin RI. 1976. Effects of vapor phase pollutants on nervous system and sensory function. In Finkel AJ, Duel WC, eds. Clinical implications of air pollution research. Acton, MA Publishing Sciences Group, 193-216. [Pg.187]

A2A receptors that are present on sensory nerves in the carotid body, aortic body and elsewhere in the periphery produce excitatory sensory input. These receptors have been implicated in the production of pain associated with angina pectoris, ulcer and the human blister base preparation. [Pg.314]

Whether subthreshold doses in animals can produce any animal neurobehavioral component of the loosening of inhibition and inner-directed attention sought for by some clinicians in using less potent drugs for a kind of psychosynthesis is uncertain. Sensitization and habituation studies implicate raphe function but not in any simple way (32), and pavlovian studies show very low dose effects on sensory processing (39,43). [Pg.112]

Handlers of methyl methacrylate cement have developed paresthesia of the fingers. Dental technicians who use bare hands to mold methyl methacrylate putty had significantly slower distal sensory conduction velocities from the digits, implicating mild axonal degeneration in the area of contact with methyl methacrylate. The toxic effect on the nervous tissues may be due to diffusion into the nerve cells causing lysis of the membrane lipids and destruction of the myelin sheath. [Pg.488]

Of the different sensory modalities, olfaction does not appear to feature in reports of the effects of plant hallucinogens. Since olfaction is the one sense not relayed through the thalamus, this brain area is likely to be central to the changes in consciousness described. Many target receptors implicated, e.g. muscarinic, 5-HT2, D2, D3 and opiate, are present in this thalamic nuclei the human brain. [Pg.222]

Talamini, L.M., Ellenbroek, R, Koch, T., Korf, J.. Impaired sensory gating and attention in rats with developmental abnormalities of the mesocortex. Implications for schizophrenia. Aim. NY Acad. ScL 911, 486-494, 2000. [Pg.367]

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. [Pg.121]


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