ライフサイエンスコーパス: aspartame

1 s ranged from 4.10 (saccharin) to 4540 L/kg (aspartame).

2 the wall materials and the intact nature of aspartame.

3 lates the higher affinity of neotame than of aspartame.

4 for the small molecule analytes caffeine or aspartame.

5 symptoms have been reported anecdotally with aspartame.

6 of ASWs sorbed to SPM was in the rank order: aspartame (50.4%) > acesulfame (10.9%) > saccharin and s

7 Significant removal of aspartame (68.2%) and saccharin (90.3%) was found in WWT

8 g hBcl-2 showed significant reduction of the aspartame amino transferase (AST) and lactate dehydrogen

9 one has been used in a brief synthesis of an aspartame analogue.

10 intakes of caffeine, sucrose, fructose, and aspartame and early menarche.

11 ian species toward the artificial sweeteners aspartame and neotame are determined by the steric effec

12 On storage (4-7 degrees C/7 days) aspartame and neotame content decreased significantly (P

13 th the isolation procedure for separation of aspartame and neotame in flavoured milk (pasteurized and

14 sfully used for the routine determination of aspartame and neotame in flavoured milk.

15 For instance, artificial sweeteners aspartame and neotame taste sweet to humans, apes, and O

16 required for recognizing sweeteners, such as aspartame and neotame.

17 of the method was approximately 98% for both aspartame and neotame.

18 0 min) resulted in approximately 40% loss of aspartame and only 8% of neotame was degraded.

19 ironmental emission of sucralose, saccharin, aspartame, and acesulfame were determined based on the c

20 ctively evaluated whether the consumption of aspartame- and sugar-containing soda is associated with

21 articles stabilized with a common sweetener, aspartame (AuNP@Ag@Asm), combine the antimicrobial prope

22 jective of this work was to microencapsulate aspartame by double emulsion followed by complex coacerv

23 This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or be

24 l kit-LC/MS performance test mix-composed of aspartame, cortisone, reserpine, and dioctyl phthalate h

25 Other popular sweeteners such as aspartame, cyclamate, and saccharin were not enhanced by

26 -times as short as 5 min, these caffeine- or aspartame-dependent ribozymes function as highly specifi

27 yl-phenylalanine-methyl ester (the sweetener aspartame, DF-OMe).

28 The first month was aspartame free.

29 intenance and follow-up, participants in the aspartame group experienced a 2.6% (2.6 kg) and 4.6% (4.

30 75 wk, respectively, whereas those in the no-aspartame group gained an average of 5.4% (5.4 kg) and 9

31 The aspartame group lost significantly more weight overall (

32 r low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group.

33 ce and follow-up (P = 0.046) than did the no-aspartame group.

34 Large daily doses of aspartame had no effect on neuropsychologic, neurophysio

35 e safety reports of the artificial sweetener aspartame, health-related concerns remain.

36 /15 min) resulted in complete degradation of aspartame; however, 50.50% of neotame remained intact.

37 that neotame exhibited better stability than aspartame in both pasteurized and in-bottle sterilized f

38 systems that were able to detect caffeine or aspartame in solution over a concentration range from 0.

39 n assigned to the aspartame-treatment group, aspartame intake was positively correlated with percenta

40 developed in controlling the release of the aspartame into the food, thus prolonging its sweetness.

41 plinary weight-control program that includes aspartame may facilitate the long-term maintenance of re

42 ffect of a constituent of diet soda, such as aspartame, on select cancers, the inconsistent sex effec

43 en consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each.

44 the fructose and glucose phases than in the aspartame phase (P < 0.003 for each), with no difference

45 Caffeine- or aspartame-responsive ribozymes were converted into fluor

46 Because the arginine-glycine-aspartame (RGD) and polylysine (pK7) motifs have been sh

47 -SD increment: 1.22; 95% CI: 1.08, 1.37) and aspartame (RR for 1-SD increment: 1.20; 95% CI: 1.10, 1.

48 onsumed beverages sweetened with HFCS at 0% (aspartame sweetened, n = 23), 10% (n = 18), 17.5% (n = 1

49 s were later given simultaneous access to an aspartame-sweetened 8.4% (vol/vol) ethanol solution and

50 s young adults, they were given access to an aspartame-sweetened 8.4% alcohol solution and vehicle fo

51 requirement, or an equivalent volume of the aspartame-sweetened beverage, and consumption was mandat

52 in individuals consuming SSBs compared with aspartame-sweetened beverages.

53 bjects consumed the fructose-, glucose-, and aspartame-sweetened beverages.

54 SD (regular cola), isocaloric semiskim milk, aspartame-sweetened diet cola, and water.

55 domly assigned to consume or to abstain from aspartame-sweetened foods and beverages during 16 wk of

56 the addition of the high-intensity sweetener aspartame to a multidisciplinary weight-control program

57 ug/L (sucralose) in effluent, and from 0.08 (aspartame) to 0.65 mug/g dw (sucralose) in sludge.

58 /L (sucralose) in wastewater influent, 0.49 (aspartame) to 27.7 mug/L (sucralose) in primary influent

59 a mean concentration that ranged from 0.13 (aspartame) to 29.4 mug/L (sucralose) in wastewater influ

60 mug/L (sucralose) in primary influent, 0.11 (aspartame) to 29.6 mug/L (sucralose) in effluent, and fr

61 oncentrations increased significantly during aspartame treatment.

62 Among women assigned to the aspartame-treatment group, aspartame intake was positive

63 Aspartame was found in 92% of influent SPM samples at a

64 might ignore follow-up, leave town, or take aspartame when instructed to take aspirin.

65 lts indicated it was possible to encapsulate aspartame with the techniques employed and that these pr