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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 ely used artificial sweeteners-sucralose and aspartame.
7 of ASWs sorbed to SPM was in the rank order: aspartame (50.4%) > acesulfame (10.9%) > saccharin and s
8                       Significant removal of aspartame (68.2%) and saccharin (90.3%) was found in WWT
9 ed drinking water containing 0.015% or 0.03% aspartame, a dose equivalent of 8 to 15% of the FDA reco
10     Three low calorie artificial sweeteners (aspartame, acesulfame potassium and sucralose), one stev
11 f the most popular NNS, including saccharin, aspartame, acesulfame potassium, sucralose, and stevia,
12                                Additionally, aspartame affected genes involved in tight and adherens
13 g hBcl-2 showed significant reduction of the aspartame amino transferase (AST) and lactate dehydrogen
14 ily and 3-dehydratases, which are related to aspartame aminotransferases.
15                  We show that consumption of aspartame, an FDA-approved artificial sweetener, daily f
16 one has been used in a brief synthesis of an aspartame analogue.
17  intakes of caffeine, sucrose, fructose, and aspartame and early menarche.
18 nd NFC (1.4 x 10(4) M(-1)), whereas sucrose, aspartame and glutamic acid did not bind at all.
19 ian species toward the artificial sweeteners aspartame and neotame are determined by the steric effec
20            On storage (4-7 degrees C/7 days) aspartame and neotame content decreased significantly (P
21 th the isolation procedure for separation of aspartame and neotame in flavoured milk (pasteurized and
22 sfully used for the routine determination of aspartame and neotame in flavoured milk.
23          For instance, artificial sweeteners aspartame and neotame taste sweet to humans, apes, and O
24 of the method was approximately 98% for both aspartame and neotame.
25 required for recognizing sweeteners, such as aspartame and neotame.
26 0 min) resulted in approximately 40% loss of aspartame and only 8% of neotame was degraded.
27 ironmental emission of sucralose, saccharin, aspartame, and acesulfame were determined based on the c
28 lower for sucralose compared with saccharin, aspartame, and rebA consumption.
29 ctively evaluated whether the consumption of aspartame- and sugar-containing soda is associated with
30  soft drinks, motivated by classification of aspartame as a possible carcinogen by the International
31 articles stabilized with a common sweetener, aspartame (AuNP@Ag@Asm), combine the antimicrobial prope
32 jective of this work was to microencapsulate aspartame by double emulsion followed by complex coacerv
33       This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or be
34 sted on existing Cl-DBP data sets related to aspartame chlorination in tap water, our ChloroDBPFinder
35 ntake may produce neurobehavioral changes in aspartame-consuming individuals and their descendants.
36 han current expectations, which only include aspartame-consuming individuals.
37 tion of the findings to humans suggests that aspartame consumption at doses below the FDA recommended
38  diazepam and gene expression data show that aspartame consumption shifted the excitation-inhibition
39 served in male and female mice consuming the aspartame-containing water.
40 l kit-LC/MS performance test mix-composed of aspartame, cortisone, reserpine, and dioctyl phthalate h
41             Other popular sweeteners such as aspartame, cyclamate, and saccharin were not enhanced by
42 paracetamol, caffeine, acetylsalicylic acid, aspartame, d-glucose, and detergent (containing perborat
43 -times as short as 5 min, these caffeine- or aspartame-dependent ribozymes function as highly specifi
44 yl-phenylalanine-methyl ester (the sweetener aspartame, DF-OMe).
45 d, erythritol (Stevia), sucralose (Splenda), aspartame (Equal), and saccharin (Sweet'N Low), only ery
46 pring in two generations descending from the aspartame-exposed males.
47                                              Aspartame exposure upregulated proinflammatory genes, pa
48                          The first month was aspartame free.
49 intenance and follow-up, participants in the aspartame group experienced a 2.6% (2.6 kg) and 4.6% (4.
50 75 wk, respectively, whereas those in the no-aspartame group gained an average of 5.4% (5.4 kg) and 9
51                                          The aspartame group lost significantly more weight overall (
52 r low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group.
53 ce and follow-up (P = 0.046) than did the no-aspartame group.
54                         Large daily doses of aspartame had no effect on neuropsychologic, neurophysio
55                                              Aspartame has been widely used as a sweetener in foods a
56 e safety reports of the artificial sweetener aspartame, health-related concerns remain.
57 /15 min) resulted in complete degradation of aspartame; however, 50.50% of neotame remained intact.
58 that neotame exhibited better stability than aspartame in both pasteurized and in-bottle sterilized f
59                                              Aspartame in commercial samples was below the limits by
60 IA-PH and DIA-CG) were developed to quantify aspartame in lemon-flavored soft drinks, motivated by cl
61 emistry, and suitable for quality control of aspartame in soft drinks.
62 systems that were able to detect caffeine or aspartame in solution over a concentration range from 0.
63 weeteners (neohesperidin dihydrochalcone and aspartame) in an Australian adolescent twin sample (n =
64  indicate that, at commonly consumed levels, aspartame induces cellular stress, inflammation and epit
65                                We found that aspartame induces cytotoxic effects, disrupts the epithe
66 n assigned to the aspartame-treatment group, aspartame intake was positively correlated with percenta
67  developed in controlling the release of the aspartame into the food, thus prolonging its sweetness.
68 plinary weight-control program that includes aspartame may facilitate the long-term maintenance of re
69  raise concerns that daily dietary intake of aspartame may pose previously underappreciated risks to
70 of beverage sweetened with sucrose (n = 39), aspartame (n = 30), saccharin (n = 29), sucralose (n = 2
71                     We report the effects of aspartame on anxiety-like behavior, neurotransmitter sig
72 ffect of a constituent of diet soda, such as aspartame, on select cancers, the inconsistent sex effec
73  reciprocally impact feeding behavior, while aspartame only activated bitter cells.
74 en consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each.
75  the fructose and glucose phases than in the aspartame phase (P < 0.003 for each), with no difference
76 ificantly increase body weight compared with aspartame, rebA, and sucralose, whereas weight change wa
77                                 Caffeine- or aspartame-responsive ribozymes were converted into fluor
78                 Because the arginine-glycine-aspartame (RGD) and polylysine (pK7) motifs have been sh
79 -SD increment: 1.22; 95% CI: 1.08, 1.37) and aspartame (RR for 1-SD increment: 1.20; 95% CI: 1.10, 1.
80 s along the paternal lineage suggesting that aspartame's adverse cognitive effects are heritable, and
81            Thus, human population at risk of aspartame's potential mental health effects may be large
82 Even so, several synthetic sweeteners (e.g., aspartame, saccharin, sucralose) are becoming less popul
83        RNA sequencing analysis revealed that aspartame significantly alters the transcriptome in gut-
84 onsumed beverages sweetened with HFCS at 0% (aspartame sweetened, n = 23), 10% (n = 18), 17.5% (n = 1
85 s were later given simultaneous access to an aspartame-sweetened 8.4% (vol/vol) ethanol solution and
86 s young adults, they were given access to an aspartame-sweetened 8.4% alcohol solution and vehicle fo
87  requirement, or an equivalent volume of the aspartame-sweetened beverage, and consumption was mandat
88 bjects consumed the fructose-, glucose-, and aspartame-sweetened beverages.
89  in individuals consuming SSBs compared with aspartame-sweetened beverages.
90 SD (regular cola), isocaloric semiskim milk, aspartame-sweetened diet cola, and water.
91 domly assigned to consume or to abstain from aspartame-sweetened foods and beverages during 16 wk of
92 the addition of the high-intensity sweetener aspartame to a multidisciplinary weight-control program
93 ug/L (sucralose) in effluent, and from 0.08 (aspartame) to 0.65 mug/g dw (sucralose) in sludge.
94 /L (sucralose) in wastewater influent, 0.49 (aspartame) to 27.7 mug/L (sucralose) in primary influent
95  a mean concentration that ranged from 0.13 (aspartame) to 29.4 mug/L (sucralose) in wastewater influ
96 mug/L (sucralose) in primary influent, 0.11 (aspartame) to 29.6 mug/L (sucralose) in effluent, and fr
97 oncentrations increased significantly during aspartame treatment.
98                  Among women assigned to the aspartame-treatment group, aspartame intake was positive
99                                              Aspartame was found in 92% of influent SPM samples at a
100  might ignore follow-up, leave town, or take aspartame when instructed to take aspirin.
101 lts indicated it was possible to encapsulate aspartame with the techniques employed and that these pr

 
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