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1 y loss of Mn-dependent superoxide dismutase (SodA).
2 of manganese-dependent superoxide dismutase sodA).
3 ter/operator region of superoxide dismutase (sodA).
4 detoxify ROS, such as superoxide dismutase (SodA).
5 D. radiodurans cells cannot be attributed to SodA.
6 tested whether the same is true for Borrelia SodA.
7 e, with negligible EPR signal from Mn(2+) of SodA.
8 comparison with men who did not consume diet soda.
9 loenzyme to degrade ROS in B. burgdorferi is SodA.
10 ed by substituting alternative beverages for soda.
11 esting that manganese regulates the level of SodA.
12 ated or decaffeinated coffee for low-calorie soda.
13 te dehydrogenase subunits PdhB and PdhD, and SodA.
14 online at https://hippocrates.duhs.duke.edu/soda.
15 levels of its manganese superoxide dismutase SodA.
16 eef, pork, or lamb sandwich to 0.99 for diet soda.
17 eas we observed no such association for diet soda.
18 Therefore, this gene was designated sodA.
19 odM, SodA, and a hybrid composed of SodM and SodA.
20 ion of SOD activity by cloned M. catarrhalis sodA.
21 ponential phase of growth, SodM more so than SodA.
22 ssense mutations in the normal stop codon of sodA.
23 ects of the long-term consumption of sugared soda.
24 stronic operon, consisting of orfY-fumC-orfX-sodA.
25 ng/d (daily consumers) of either SSB or diet soda.
26 ceived intolerance to spicy foods, coffee or soda.
27 (2+) speciation, despite the paucity of holo-SodA.
28 calories in quickly ingested drinks such as sodas.
29 dolescents and with higher intake of regular soda (73.77 g and 88.28 g for children and 163.67 g and
30 pared with women who consumed less sweetened soda (86.5 pg/mL compared with 74.4 pg/mL, P = 0.01) aft
31 umarase C, Mn-dependent superoxide dismutase SodA, a ferredoxin and ferredoxin reductase and several
36 onensis metacyclic promastigotes lacking one SODA allele failed to replicate in macrophages and were
38 s between the superoxide-detoxifying enzyme (SodA), an integral membrane protein (DoxX), and a predic
39 per 100,000 person-years for sugar-sweetened soda and 14 and 47 cases per 100,000 person-years for or
42 tions among white women, whereas caffeinated soda and green tea intakes were associated with increase
45 drates, less protein, and more caffeine-free soda and juice than whites did during the study (Ps < 0.
46 quire manganese in turn promotes function of SodA and KatN, enzymes that use the metal as a cofactor
49 f fragments of two other housekeeping genes, sodA and mutS, confirmed that the isolates are most clos
50 ctose-rich beverages such as sugar-sweetened soda and orange juice can increase serum uric acid level
54 of phenazine methosulfate or by deletion of sodA and sodB, stimulates rugose biofilm formation in th
58 and DNA sequencing of the housekeeping gene sodA and the putative virulence gene hylB differentiated
59 = 0.003), with +1.09 cent/oz (p < 0.001) for sodas and energy drinks, but a lower change in other cat
60 ule, reacted with T. cruzi mitochondrial (Fe-SODA) and cytosolic (Fe-SODB) SODs with second order rat
61 f cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) bever
64 different types of SCBs (i.e., fruit juice, soda, and concentrate).We included 3312 mother-child pai
65 otein was not detected in macrophages; sodC, sodA, and fbpB transcription showed no decrease; and acr
67 ing 54 VGS strains for which MLSA, 16S gene, sodA, and gyrB data are available at the NCBI, showing t
71 ciation of soda, including specific types of soda, and risk of hip fracture in postmenopausal women.
73 SodA to the periplasm, ruling out export of SodA as a complex with a TAT substrate as a chaperone.
74 utant, we identified superoxide dismutase A (SodA) as a protein dependent on SecA2 for secretion.
76 he gene encoding for superoxide dismutase A (sodA, bb0153), an enzyme mediating the dismutation of su
77 sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal
78 resulted in nitration and inactivation of Fe-SODA but not Fe-SODB, suggesting that these enzymes play
81 n of other caffeinated products (caffeinated soda, caffeinated tea, decaffeinated coffee or chocolate
83 requency of consumption of unhealthy snacks (soda, candy, and potato chips) from 2001 to 2008 in Norw
84 respectively, more in BMI than the juice and soda cluster across the study interval in a multivariate
86 ndicates that M. catarrhalis strains lacking SodA constitutively express immunogenic OMPs previously
91 Our objective was to examine patterns of soda consumption and substitution of alternative beverag
94 puted RRs for hip fractures by the amount of soda consumption by using Cox proportional hazards model
96 Recent studies have examined sugar-sweetened soda consumption in relation to early markers of kidney
97 The absence of apparent effects of sugared soda consumption in younger people may also be related t
104 a, significant associations between DMFS and soda consumption were generally seen in persons over age
107 07-2008, primarily because of a reduction in soda consumption, mean intakes continue to exceed recomm
109 pants were randomly assigned to consume diet soda containing sucralose or carbonated water (control)
110 rranted, particularly of the precise role of sodas containing artificial sweeteners in bladder sensat
111 consumed >/=1 cup (1 cup = 237 mL) sweetened soda/d had 16.3% higher estradiol concentrations compare
112 who consumed >/=1 serving of sugar-sweetened soda/d had a 63% (HR: 1.63; 95% CI: 1.15, 2.30; P-trend
113 (RR for consumption of >/=1 serving of diet soda/d when the 2 cohorts were pooled: 1.42; 95% CI: 1.0
114 Compared with 1 serving of sugar-sweetened soda/d, 1 serving of decaffeinated coffee/d was associat
115 stroke for >/= 1 serving of sugar-sweetened soda/d, compared with none, was 1.16 (95% CI: 1.00, 1.34
116 otal stroke for >/= 1 serving of low-calorie soda/d, compared with none, was 1.16 (95% CI: 1.05, 1.28
117 development of metacyclic promastigotes, as SODA/DeltasodA cultures were strongly depleted in this i
118 itochondrial oxidative damage and failure of SODA/DeltasodA promastigotes to differentiate into axeni
121 uit drinks) and artificially sweetened (diet sodas, diet drinks) beverages from food-frequency questi
122 we demonstrate that a bulk of B. burgdorferi SodA directly associates with manganese, and a smaller p
123 ncer risk in individuals who consume regular soda do not permit the ruling out of chance as an explan
124 nducing agent, methyl viologen, but the sarA sodA double mutant was more resistant to the same stress
127 caries increment were higher consumption of soda drinks, older age of child, greater weight-for-age,
134 manganese, greatly reduced SOD activity and SodA expression, suggesting that manganese regulates the
137 foods consumed with the television off, less soda, fast food, fruit, and vegetables were consumed wit
138 We observed 3 dietary patterns: juice and soda; fast food and fruit drinks; and fruit, vegetable,
139 t, we cloned the homologous genes (glnA1 and sodA) from the rapid-growing, nonpathogenic Mycobacteriu
141 atively averaged intakes of sugar-sweetened (sodas, fruit punches, lemonades, fruit drinks) and artif
143 include those encoding superoxide dismutase (sodA), fumarate dehydratase (fumC), bacterioferritin (bf
151 d soda intake, particularly caffeinated diet soda, had higher symptom scores, urgency, and LUTS progr
155 In addition, the superoxide dismutase gene (sodA) has been identified as a potential target for spec
156 hioredoxin that either participate directly (SodA, HPI, and AhpC) or have key regulatory functions (F
160 to quantify SY in isotonic drinks and orange sodas, in the range of 7.8-39.7 mg L(-1), with relative
162 with limited power, neither regular nor diet soda increased risk of leukemia but were associated with
163 However, in men, >/=1 daily serving of diet soda increased risks of NHL (RR: 1.31; 95% CI: 1.01, 1.7
164 icular, Cys(83) mutation (C83S, absent in Fe-SODA) increased the Fe-SODB sensitivity toward peroxynit
168 escents and (2) among adolescents, increased soda intake was twice as large when fast food was consum
170 t) of Kool-aid, fruit juices, and nondietary soda intake, expressed as servings per week, and classif
175 h previous work suggests that B. burgdorferi SodA is an iron-dependent superoxide dismutase (SOD), la
176 n at moderate consumption amounts, sweetened soda is associated with elevated follicular estradiol co
177 nsumption of aspartame- and sugar-containing soda is associated with risk of hematopoetic cancers.
179 mption of sugar-sweetened soda, but not diet soda, is associated with increased risk of seropositive
180 s within mycobacterial superoxide dismutase (SodA), L-alanine dehydrogenase (AlaDH), and L-glutamine
184 can be detoxified by cytoplasmic lactoccocal SodA led to the finding that host antimicrobial-mediated
185 ue by performing (11)B NMR measurements on a soda lime borate glass that has been pressure-quenched a
186 induced changes in macroscopic properties of soda lime borate glasses compressed up to ~0.6 GPa are n
187 and carbon monoxide (CO) may be generated in soda lime canisters and may be inhaled by patients.
190 d, include the degradation of both agents by soda lime under certain circumstances during closed circ
192 this is because of Mg out-diffusion from the soda-lime glass substrates and is not disadvantageous to
196 emical and physical properties of commercial soda-lime slides affect the ability of these slides to b
198 bust, and spontaneous graphene n-doping on a soda-lime-glass substrate via surface-transfer doping fr
199 onductor that itself has been deposited onto soda-lime-glass, via surface-transfer doping from Na ato
201 The unique properties of B. burgdorferi SodA may represent adaptation to expression in the manga
202 ermination identified the disrupted genes as sodA (Mn-containing superoxide dismutase), fpr (NADPH:fe
204 complete attenuation of infectivity for the sodA mutant compared with control strains at 21 days pos
209 However, only the viability of the sodM sodA mutant was reduced when MV was added during the lat
211 r percentage of cell death upon treatment of sodA mutant with superoxide generators compared with its
215 Mycobacterium smegmatis, generated glnA1 and sodA mutants of M. smegmatis by allelic exchange, and qu
218 gene expressed from a plasmid complemented a sodA mutation in S. aureus, and the protein formed a hyb
220 sis Our inability to generate L. amazonensis SODA null mutants and the lethal phenotype observed foll
224 es of total SCBs and fruit juice, but not of soda or concentrate, were associated with a higher FMI [
228 mediated silencing of the Trypanosoma brucei SODA ortholog suggests that SODA is essential for trypan
229 .001), fried foods (P(trend)=0.02), and diet soda (P(trend)=< 0.001) also were adversely associated w
231 ble models, each additional serving of total soda per day was associated with a significant 14% incre
233 This study demonstrates that M. catarrhalis SodA plays a critical role in the detoxification of endo
234 cycling compound that produces ROS, and that SodA plays a protective role against the streptonigrin.
243 oth hybrid SOD forms as well as the SodM and SodA proteins of S. aureus and the S. epidermidis SodA p
244 and produced lower levels of NapA (Dps) and SodA, proteins involved in the oxidative stress response
245 crobial-mediated lysis is a prerequisite for SodA release and SodA's extracytoplasmic O2 (-) scavengi
246 soda (RR: 1.19; 95% CI: 1.02, 1.38) and diet soda (RR: 1.12; 95% CI: 1.03, 1.21) and also did not sig
247 cantly elevated in consumers of both regular soda (RR: 1.19; 95% CI: 1.02, 1.38) and diet soda (RR: 1
248 However, in all three cases (whisky and club soda; rum with cola; gin and tonic water), MEC was quick
251 nce, full-length and 5' partial 16S gene and sodA sequence analyses failed to correctly assign all st
252 howing that gyrB is superior to 16S gene and sodA sequence analyses for VGS species identification.
253 (i) EcoRI ribotyping, combined with hylB and sodA sequencing, provides a discriminatory subtype analy
255 endogenous level of H2S is reduced in fur or sodA sodB cells but restored after the addition of an ir
259 d rescued an Escherichia coli double mutant (sodA sodB) under conditions that are otherwise lethal.
260 ons were 0.2, 0.3, 0.8, and 1.9 mM for arsB, sodA sodB, crc, and gor mutants, respectively, and were
261 e aerobic growth defects of E. coli QC774, a sodA sodB-deficient mutant, demonstrated the functional
263 is GSs (in the glnA1 strain) or SODs (in the sodA strain), in contrast to previous observations in wi
265 detrimental effect of a constituent of diet soda, such as aspartame, on select cancers, the inconsis
266 high manganese is necessary to activate the SodA superoxide dismutase (SOD) essential for virulence.
269 hypothesis, we examined the specific role of SODA, the mitochondrial SOD isoform in Leishmania amazon
270 than 1 serving per month of sugar-sweetened soda, the multivariate relative risk of gout for 1 servi
272 to deliver antioxidant, colitis-attenuating SodA to the inflamed intestinal mucosa, and host antimic
274 A tatC mutant of R. l. bv. viciae exported SodA to the periplasm, ruling out export of SodA as a co
277 y MarA resulted in greater marRAB and lesser sodA transcription than did saturation by SoxS, implying
278 r aerobic conditions, the levels of sodM and sodA transcription, in particular the sodM transcript, a
279 isolates), ATPase (types IA1, IA2, and IC), sodA (types IA2 and IB), atpD (type II), and recA (type
281 ed amino acid sequence of the S. epidermidis sodA was 92 and 76% identical to that of the SodA and So
282 c conditions, transcription of both sodM and sodA was considerably enhanced in the sarA mutant compar
289 nsumption of sugar-sweetened and low-calorie sodas was associated with a significantly higher risk of
290 e cola, and other sugar-sweetened carbonated soda) was obtained from a validated food-frequency quest
291 d the gene responsible for the SOD activity, sodA, was isolated from a recent pediatric clinical isol
292 he manganese-dependent superoxide dismutase, SodA, was significantly less virulent than wild-type in
293 s well as high-fructose corn syrup-sweetened soda, we see the pervasive influence of corn as an ingre
294 ed meat, processed meat, and sugar-sweetened soda were computed with responses to a 120-item food-fre
295 4, P = 0.02) and the frequent consumption of soda were positively associated with visceral obesity (O
296 The 10 N-terminal amino acid residues of SodA were sufficient to target the reporter protein alka
297 subset of its target mRNAs (fdoG, nuoA, and sodA), whereas the sodB and sdhC targets are barely affe
298 s the need for import and storage of caustic soda, which typically represents a cost and a hazard.
300 om low-symmetry enzyme sites such as that of SodA, with a minority pool of LMW Mn(2+) complexes that
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