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21.
Effect of temperature, pH, and ions on sweet taste   总被引:1,自引:0,他引:1  
The purpose of this experiment was to determine the effects of temperature (50 degrees C and 6 degrees C), pH (pH 3.0, 4.0, 5.0, 6. 0, and 7.0) and the addition of monovalent and divalent cations (5 mM Na(+), 5 mM K(+), and 5 mM Ca(2)+ ) on the sweetness intensity ratings of sweeteners ranging widely in chemical structure. A trained panel provided intensity evaluations for prototypical tastes (sweet, bitter, sour, and salty) as well as aromatic and mouth-feel attributes. The following sweeteners were included in this experiment: three sugars (fructose, glucose, sucrose), three terpenoid glycosides (monoammonium glycyrrhizinate, rebaudioside-A, stevioside), two polyhydric alcohols (mannitol, sorbitol), two dipeptide derivatives (alitame, aspartame), two N-sulfonylamides (acesulfame-K, sodium saccharin), one sulfamate (sodium cyclamate), one protein (thaumatin), one dihydrochalcone (neohesperidin dihydrochalcone), and one chlorodeoxysugar (sucralose). Two to five levels of each sweetener reflecting a range of sweetness intensities were tested, using formulae developed by DuBois et al. The main finding from this three-part study was that temperature, pH, and ions had little effect on perceived sweetness intensity. Even when significant differences were found in the temperature study, the effects were very small.  相似文献   
22.
Campylobacter pyloridis was isolated from 77% of 220 (35%) unselected adults undergoing gastroscopy. Isolation was significantly associated with histological gastritis (p less than 0.0001), duodenal ulcer (p less than 0.0001), and to a much lesser extent, with gastric ulcer (p less than 0.05). The relation between the isolation of C pyloridis and peptic ulcer seemed to be independent of coexisting gastritis. In those with no endoscopic or histological evidence of disease there was no relation between isolation and increasing age. Antibody responses to a whole cell sonicate of a strain of C pyloridis were measured by means of an enzyme linked immunosorbent assay (ELISA). Increased IgA (p less than 0.0001) and IgG (p less than 0.0001) antibody titres were found in patients with C pyloridis. Peptic ulceration or gastritis were present in 78% and 100% of patients with a high concentration of IgG and IgA, respectively, but in only 9% and 18% of those with low titres. These results provide further evidence for a possible pathogenic role of these organisms in gastric disease and suggest that immunological markers of their presence might be useful non-invasive indicators of disease.  相似文献   
23.
Clark  P.  Holz  P.  Booth  R.  Jakob-Hoff  R.  Cooper  D.W.  Boardman  W.S.  Parry  B.W.  Norman  R.J. 《Comparative clinical pathology》2003,12(1):11-16
 Blood was collected from 31 Parma wallabies from five different captive populations. The morphology of erythrocytes, leucocytes and platelets was similar to that previously described for macropodids. The effects of location (population), anaesthesia and analyser on the haematological characteristics of the wallabies were considered. Location had an affect on many of the values, anaesthesia affected some of the leucocyte values, and analyser had little effect. Received: 22 November 2002 / Accepted 13 February 2003 Acknowledgements We thank Mrs R. Power, Ms S. Bayliss, Ms T. Smith and Mrs P. Slack for technical assistance, Mr D. Hopcroft for assistance with electron microscopy and Mr D. Hedderly for performing the statistical analyses.  相似文献   
24.
We have examined the mutational specificity of 1-nitroso-6-nitropyrene(1,6-NONP), an activated metabolite of the carcinogen 1,6-dinitropyrene,in the lacI gene of Escherichia coli strains which are deficientin nucleotide excision repair (strain NR6113,  相似文献   
25.
The human pineal gland is an extremely active neuroendocrine transducer. Environmental light acts through the retina and entrains the pineal gland's circadian rhythms by way of the hypothalamus and sympathetic nervous system. Light depresses pinealocyte activity. It is possible to do without the pineal, but this tiny gland is considered to be the "regulator of regulators" and important in general homeostasis. A direct retino-hypothalamic pathway is probably involved; and a system of synchronizing potentially independent oscillators is postulated.  相似文献   
26.
Eighty-one cementless Trilock (Depuy, Warsaw, IN) femoral components were observed for 2 to 6 years. The following end points were examined: revision (none), pain score less than 5 (six patients), and radiographic settling greater than 5 mm (three patients). Four patients (5%) had thigh pain at follow-up. No complete radiopaque lines could be identified around the porous surface of the femoral components. By any standard, the wedge-fit tapered cementless femoral design is successful. As the follow-up period lengthens, a survivorship analysis can be done to assess the long-term potential of the Trilock design.  相似文献   
27.
  1. The role of the vasculature and calcitonin gene-related peptide (CGRP) in nitroglycerin (NTG)-mediated platelet inhibition was studied.
  2. In vitro incubations of CGRP in whole blood induced a dose-dependent inhibition of platelet aggregation with an IC50 of 62.1 nM.
  3. The platelet inhibition induced by CGRP was blocked by co-incubation of 0.53 μM CGRP8-37, as well as 30 μM NG-nitro-monomethyl-L-arginine (L-NMMA).
  4. In a separate group of experiments, 100 nM NTG in rat whole blood (WB) induced platelet inhibition of 6.0±1.3% (mean±s.d.), which was enhanced to 77.6±3.5% by the addition of rat aortic tissue (AT) (P<0.001). The inclusion of CGRP8-37 with NTG and AT in WB reduced platelet inhibition to 31.6±6.8% (P<0.01). Incubation of WB and AT with 30 μM L-NMMA reduced NTG-induced inhibition of platelet aggregation to 26.4±4.2% (P<0.001).
  5. It is concluded that vascular tissue contributes to the antiplatelet mechanism of action of NTG. Furthermore, NTG apparently evokes the release of CGRP from vascular tissue and this neuropeptide contributes to the antiplatelet actions of NTG.
  6. The antiplatelet activity of CGRP in whole blood is mediated primarily through the activation of nitric oxide synthase.
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