ライフサイエンスコーパス: DHA

1 DHA administered with CAGE was retained in the intestine

2 DHA is a key central nervous system constituent and the

3 DHA supplementation did not change the lipogenic index o

4 DHA supplementation increased (P < 0.05) plasma EPA conc

5 DHA supplementation reduced blood triglycerides (0.85 +/

6 DHA upregulated the expression of anti-oxidative enzymes

7 DHA was confined to these lipids, while plastidial lipid

8 DHA was mainly found in the phospholipid fraction in all

9 ing nanocarriers (nanoARVs) containing 5-15% DHA were 90-140 nm in size, had high darunavir payload (

10 maresin 1, 17S-hydroxy-4Z,7Z,10Z,13Z,15E,19Z-DHA, and 14S-hydroxy-4Z,7Z,10Z,12E,16Z,19Z-DHA were evid

11 D1, 10S,17S-dihydroxy-4Z,7Z,11E,13E,15Z,19Z-DHA (10S,17S-diHDHA), maresin 1, 17S-hydroxy-4Z,7Z,10Z,1

12 Z-DHA, and 14S-hydroxy-4Z,7Z,10Z,12E,16Z,19Z-DHA were evident in females, and lower cortical 17R-reso

13 class A (TEM-1, CTX-M-2) and class C (CMY-2, DHA-1) enzymes, is reported.

14 ocosahexaenoic acid, DHA (66%-lipid with 27%-DHA).

15 European Union must contain 20-50 mg omega-3 DHA (22:6n-3) per 100 kcal, which is equivalent to about

16 f 20:5n-3 (EPA), 22:5n-3 (DPA), and 22:6n-3 (DHA) on the bacterial community.

17 sis of erythrocyte EPA [20:5n-3 (omega-3)] + DHA (22:6n-3) and serum triacylglycerol, LDL and HDL cho

18 Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine int

19 , we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage.

20 condition characterized by formation of 2,8-DHA crystals within renal tubules.

21 the cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical rele

22 Adenine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease,

23 g had no effect on the manifestations of 2,8-DHA nephropathy.

24 transferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by form

25 Feeding mice a DHA-enriched diet alleviated most pathologies.

26 concentrations of the 4 fatty acids (LA, AA, DHA, and EPA) were measured in maternal plasma.

27 yperpolarized [1-(13)C]dehydroascorbic acid (DHA) reduction, which can be measured in vivo using non-

28 he omega-3-fatty acid, docosahexaenoic acid (DHA) 22:6 n-3, is an important food component for the vi

29 ospholipids containing docosahexaenoic acid (DHA) are greatly enriched in the nervous system, with th

30 taenoic acid (EPA) and docosahexaenoic acid (DHA) could lead to distinct activities, there are no cli

31 Docosahexaenoic acid (DHA) has been shown to have significant neuroprotective

32 osapentaenoic acid and docosahexaenoic acid (DHA) in farmed fish have more than halved in the last 20

33 ghest concentration of docosahexaenoic acid (DHA) in our bodies, and it has been long assumed that th

34 taenoic acid (EPA) and docosahexaenoic acid (DHA) increase systemic concentrations of n-3 PUFA-derive

35 Docosahexaenoic acid (DHA) is a long-chain polyunsaturated fatty acid that has

36 Docosahexaenoic acid (DHA) is a omega-3 fatty acid typically obtained from the

37 pentaenoic acid (EPA), docosahexaenoic acid (DHA) or stearic acid (SA).

38 hat the end product of docosahexaenoic acid (DHA) oxidation, 2-(omega-carboxyethyl)pyrrole (CEP), ser

39 ed fatty acids such as docosahexaenoic acid (DHA) positively affect the outcome of retinopathy of pre

40 ved factor (PEDF) plus docosahexaenoic acid (DHA) promotes corneal nerve regeneration; here, we repor

41 taenoic acid (EPA) and docosahexaenoic acid (DHA) reduce cardiovascular risk.

42 the omega-3 fatty acid docosahexaenoic acid (DHA) reduces risk of Alzheimer's disease (AD) and amelio

43 Maternal docosahexaenoic acid (DHA) supplementation may prevent bronchopulmonary dyspla

44 the endogenous agonist docosahexaenoic acid (DHA) to examine the mechanisms of FFA4-L phosphorylation

45 % RBC membrane docosahexaenoic acid (DHA) was reduced in FMPD offspring vs. control offspring

46 aenoic acid (DPA), and docosahexaenoic acid (DHA) were inversely correlated with insulin-resistance m

47 taenoic acid (EPA) and docosahexaenoic acid (DHA) were recommended (at a dose of 2-4 g/d) for reducin

48 taenoic acid (EPA) and docosahexaenoic acid (DHA) with 440.2, 343.7 and 313.9 mg EPA + DHA/100 g raw

49 ral omega-3-fatty acid docosahexaenoic acid (DHA), 10 S,17 S-diHDHA (also referred to as protectin DX

50 tudies performed using docosahexaenoic acid (DHA), a model fat molecule, show that CAGE forms particl

51 Topical application of docosahexaenoic acid (DHA), a representative omega-3 PUFA, in wild type hairle

52 how that deficiency in docosahexaenoic acid (DHA), an essential omega-3 fatty acid, can constrain fre

53 ns have suggested that docosahexaenoic acid (DHA), an n-3 long-chain polyunsaturated fatty acid, migh

54 efits of incorporating docosahexaenoic acid (DHA), an omega-3 fatty acid essential for brain developm

55 arachidonic acid (AA), docosahexaenoic acid (DHA), or eicosapentaenoic acid (EPA), and (2) the enzyme

56 -linolenic acid (ALA), docosahexaenoic acid (DHA), rumenic acid (RmA), and alpha-eleostearic acid (al

57 eefold reduction in di-docosahexaenoic acid (DHA)-containing phospholipid species.

58 aenoic acid (EPA)- and docosahexaenoic acid (DHA)-derived specialized proresolving mediators (SPMs) i

59 eal and whole cells of docosahexaenoic acid (DHA)-rich Schizochytrium sp. as substitute for fish oil.

60 nd cis-4,7,10,13,16,19-docosahexaenoic acid (DHA).

61 to efficiently produce docosahexaenoic acid (DHA).

62 aric acid [C18:0]) and docosahexaenoic acid (DHA)[C22:6n-3] in order to increase its lipophilicity.

63 c acid (EPA, 6.3%) and docosahexaenoic acid (DHA, 1.6%), both omega-3 FAs.

64 (MFRP) participates in docosahexaenoic acid (DHA, 22:6) enrichment in a manner similar to adiponectin

65 tty acids (FAs) [e.g., docosahexaenoic acid (DHA, 22:6n-3) and eicosapentaenoic acid (EPA, 20:5n-3)],

66 Docosahexaenoic acid (DHA, 22:6n-3) supplementation in the prenatal period is

67 5omega-3) (6-fold) and docosahexaenoic acid (DHA; 22:6omega-3) (33%) in relation to control mice.

68 aenoic acid [DPA], and docosahexaenoic acid [DHA]) were evaluated with PFTs (FEV(1), FVC, and FEV(1)/

69 sp., is rich source of docosahexaenoic acid, DHA (66%-lipid with 27%-DHA).

70 ) biosynthesized from docosahexaenoic acids (DHAs) including resolvins (Rvs), protectins, and maresin

71 Reduced triglyceride concentrations after DHA supplementation are associated with increased LPL ac

72 positive cells was significantly lower after DHA treatment, and this occurred in parallel with an inc

73 The FDA-approved DNA hypomethylating agents (DHAs) like 5-azacytidine (5AC) and decitabine (DAC) demo

74 nted diets increased the egg content in ALA, DHA, RmA, as well as alpha-ESA or PunA.

75 oxygenase (LOX) activity rather than altered DHA cellular uptake.

76 st report to identify the nucleoside analogs DHAs as activators of SIRT6.

77 ucleoside analogs and non-nucleoside analogs DHAs on DNA methylation reversal using DNA pyrosequencin

78 st the combination of the nucleoside analogs DHAs with SIRT6 inhibitors or chemotherapeutic agents in

79 E. coli strains carrying class C (CMY-2 and DHA-1) and class A (TEM-1 and CTX-M-2) beta-lactamase en

80 AL and DHA-PQ remain effective for the treatment of malaria in

81 ain barrier (BBB) via passive diffusion, and DHA-lysoPC is transported across the inner membrane leaf

82 DPA and DHA were positively associated with FEV(1) and FVC (P <

83 mega-3 PUFA, particularly ALA, EPA, DPA, and DHA of broiler chicken meat due to the corresponding inc

84 EPA and DHA also improved intestinal barrier function, indicated

85 EPA and DHA also inhibited protein expression of caspase-3 and c

86 ndings on primarily diet-derived n-3 EPA and DHA and n-6 LA do not provide strong evidence to suggest

87 g MO and MU increased the content of EPA and DHA and the level of secondary oxidation products but be

88 P = 0.003, respectively), as did the EPA and DHA content in adipose tissue (P < 0.0001 and P < 0.0001

89 lmitate)f).In the omega-3 group, the EPA and DHA contributions to plasma free fatty acids increased (

90 his study tested the hypothesis that EPA and DHA could alleviate DON-induced injury to intestinal por

91 Moreover, EPA and DHA decreased cell necrosis demonstrated by live cell im

92 As EPA and DHA differentially impact cutaneous inflammation through

93 d that it is feasible to reduce ARA, EPA and DHA down to 0.43, 6.6 and 8.4% total fatty acids, respec

94 Finally, EPA and DHA downregulated protein expressions of necroptosis rel

95 To optimize EPA and DHA enrichment and bioaccessibility, the type of fish oi

96 saturated fatty acids (PUFA) such as EPA and DHA exert beneficial effects on intestinal integrity in

97 signed to different daily intakes of EPA and DHA for 12 mo.

98 16 S rRNA sequencing suggested that EPA and DHA had a greater contribution to the action of marine l

99 ted with the dose and the content of EPA and DHA in blood lipid pools.

100 Fish oil markedly enhanced EPA and DHA in mouse skin within 2 weeks, and this increase plat

101 re diploids had higher percentage of EPA and DHA in their muscle tissue (filets) compared to that of

102 ial triglyceride-lowering effects of EPA and DHA is warranted in both normolipidemic and hyperlipidem

103 The highest bioaccessibility of EPA and DHA occurred in cooked samples enriched with MO after pr

104 s set by The Global Organization for EPA and DHA Omega-3s for peroxide and/or p-anisidine value sugge

105 t excluding the potential benefit of EPA and DHA on glucose-insulin homeostasis given the inverse ass

106 Nevertheless, the contents of EPA and DHA per mass of the filets in diploid and triploid speci

107 These results suggest that EPA and DHA prevent DON-induced intestinal cell injury and enhan

108 EPA and DHA promoted cell growth indicated by higher cell viabil

109 We compared the effects of EPA and DHA supplementation on serum triglycerides, markers of l

110 ornutum, accumulating high levels of EPA and DHA together with recombinant proteins: the fungal Asper

111 ong-chain omega-3 (n-3) fatty acids (EPA and DHA) raise erythrocyte EPA + DHA [omega-3 index (O3I)] c

112 (p < 0.05) with better retention of EPA and DHA, particularly in US nanoliposomes.

113 ase linearly with elevated intake of EPA and DHA.

114 ease with dose was observed for all EPA- and DHA-derived oxylipins.

115 um, PfDegP, similarly lowers heme levels and DHA susceptibility.

116 DHA-dependent beta-arrestin recruitment and DHA-dependent extracellular-signal regulated kinase-1/2

117 that functional fat-1 and topically applied DHA potentiate cellular defense against UVB-induced skin

118 anisms of FFA4-L phosphorylation, as well as DHA-dependent beta-arrestin recruitment and DHA-dependen

119 We found even stronger associations between DHA and 38 operational taxonomic units (OTUs), the stron

120 Increases in maternal blood DHA concentration in pregnancy were related to higher IQ

121 Maternal blood DHA concentrations at delivery were unrelated to outcome

122 Increases in maternal blood DHA during pregnancy were related to verbal and full sca

123 nt and follow-on formula should provide both DHA and AA.

124 Enriching brain DHA is believed to be beneficial for the prevention and

125 asma BDNF may be used as biomarker for brain DHA enrichment.

126 s the lack of a reliable biomarker for brain DHA.

127 ed SPMs and age-associated decrease in brain DHA in APOE4 female mice.

128 line (LPC)-DHA significantly increases brain DHA, which results in increase of brain BDNF.

129 We altered the brain DHA in rats and mice over a wide range using different d

130 (phosphorylated CREB) was also increased by DHA and EPA but not by SA.

131 g their ability to be chemically modified by DHA.

132 t not the M0 or M2 phenotype, was reduced by DHA, but the phagocytic activation was not altered.

133 tion documented reduced light sensitivity by DHA-deprived retinas.

134 sit that the difference is that fish contain DHA in phospholipid form, whereas fish oil supplements d

135 d an APOE4 genotype, with decreased cortical DHA and a number of SPMs, which together may contribute

136 A 10% lower cortical DHA was evident in APOE4 females at 18 mo compared with

137 In rat spinal primary microglia cultures, DHA reduced the phagocytic response to myelin, which was

138 s for 12 wk: 1) olive oil control, 2) ~3 g/d DHA, or 3) ~3 g/d EPA.

139 DegP2, lowers porphyrin levels and decreases DHA susceptibility, without significantly altering paras

140 ivities of both intracellular dehydrogenase (DHA) and extracellular alpha-glucosidase (alpha-Glu) and

141 (P > 0.05) but did increase plasma delta13C-DHA (-27.9 +/- 0.2 to -25.6 +/- 0.1, P < 0.05) toward de

142 pid form called lysophosphatidylcholine DHA (DHA-lysoPC).

143 ees C) for oxidizing 9,10-dihydroanthracene (DHA) compared to diamond core complexes of other first-r

144 ir reactivity toward 9,10-dihydroanthracene (DHA), and a Hammett correlation was found between the se

145 , 7321) with cyclohexane, dihydroanthracene (DHA), and xanthene (Xan), we show here that KIE is a sel

146 rate constants k(2)(9,10-dihydroanthracene; DHA) = 0.485 M(-1) s(-1) and k(2)(fluorene) = 0.102 M(-1

147 ntline antimalarial drug dihydroartemisinin (DHA) at the trophozoite stage resulted in a ~ fourfold i

148 blethal concentration of dihydroartemisinin (DHA), we uncover the putative transporter Tmem14c whose

149 CKD), characterized by 2,8-dihydroxyadenine (DHA) renal parenchymal crystal deposition.

150 Monomer formation from dimeric DHA has previously been suggested as the rate-determinin

151 eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, and lowers the nutritional value due to the

152 High-dose DHA supplementation in APOE4 carriers before the onset o

153 High-dose DHA supplementation of infants born at <33 wk gestation

154 birth to 7 y CA compared with standard-dose DHA.

155 howed dose-dependency with erythrocyte EPA + DHA (r = -0.15, P = 0.04), whereas HDL showed a tendency

156 acids (EPA and DHA) raise erythrocyte EPA + DHA [omega-3 index (O3I)] concentrations, but the magnit

157 id percentage-point higher erythrocyte EPA + DHA in the fish group (P < 0.001).

158 sh [1, 2, or 4 portions/wk with 3.27 g EPA + DHA (1:1.2, wt:wt) per portion] or placebo.

159 p estimate the O3I response to a given EPA + DHA dose and chemical form.

160 d (DHA) with 440.2, 343.7 and 313.9 mg EPA + DHA/100 g raw fillet respectively among the studied fish

161 ncentration of 4.9%, given 850 mg/d of EPA + DHA EE would be ~6.5% (95% CI: 6.3%, 6.7%).

162 s to model the effects of supplemental EPA + DHA on the O3I.

163 Individuals supplemented with EPA + DHA (n = 846) took a mean +/- SD of 1983 +/- 1297 mg/d,

164 nce 2002, prescription agents containing EPA+DHA or EPA alone have been approved by the US Food and D

165 t of very high triglycerides with 4 g/d, EPA+DHA agents reduce triglycerides by >=30% with concurrent

166 We conclude that prescription n-3 FAs (EPA+DHA or EPA-only) at a dose of 4 g/d (>3 g/d total EPA+DH

167 results of a trial of 4 g/d prescription EPA+DHA in hypertriglyceridemia are anticipated in 2020.

168 A-only) at a dose of 4 g/d (>3 g/d total EPA+DHA) are an effective and safe option for reducing trigl

169 cological doses of n-3 FAs (>3 g/d total EPA+DHA) on the basis of new scientific data and availabilit

170 treat hypertriglyceridemia, n-3 FAs with EPA+DHA or with EPA-only appear roughly comparable for trigl

171 ow that the increase in plasma EPA following DHA supplementation in humans does not occur via retroco

172 ents to assess n-3 PUFA metabolism following DHA or EPA supplementation in humans.

173 IMECs required MFSD2A, which is required for DHA retention and metabolism in the gut vasculature.

174 Free DHA is transported across the outer membrane leaflet of

175 HA is metabolized to nonesterified DHA (free DHA) or a phospholipid form called lysophosphatidylcholi

176 rriers have impaired brain transport of free DHA but not of DHA-lysoPC, as a consequence of a breakdo

177 lipid vesicles to mitochondria isolated from DHA-fed mice, rescued the major losses in the mitochondr

178 lp to identify the optimal timing for future DHA clinical trials.

179 wk: 1) olive oil, 2) ~3 g EPA/d, and 3) ~3 g DHA/d.

180 Infants were given high-DHA (~1% total fatty acids) or standard-DHA (~0.3% total

181 f infants born at <33 wk gestation with high-DHA compared with standard-DHA enteral feeds decreases t

182 and the association was attenuated by higher DHA levels (P(SNPxDHA interaction) = 2.1 x 10(-7); beta(

183 dels of hCMEC/d3 cells, nanoARVs with higher DHA content achieved increased nanocarrier uptake and up

184 HA-derived monohydroxy fatty acid 17-hydroxy-DHA (HDHA) and unbalanced formation of SPMs (in particul

185 ing lipid mediators (SPMs), e.g., 17-hydroxy-DHA and 18-hydroxy-EPA.

186 sk of allergic disease, but it is unknown if DHA supplementation reduces the risk of childhood allerg

187 dy, we analyzed the consequences of impaired DHA transport across the blood-retina barrier.

188 for ELOVL2 (Elovl2(-/-) ), the key enzyme in DHA synthesis.

189 analyze photoreceptor health and function in DHA-deprived retinas using the Mfsd2a knock-out mouse as

190 decrease was associated with a reduction in DHA-phosphatidylethanolamine.

191 e (LPC) (40 mg DHA/kg) for 30 days increased DHA content of the brain by >2-fold.

192 ansporter Tmem14c whose disruption increases DHA susceptibility.

193 Instead, DHA increased the concentration of the downstream specia

194 d not affect the conversion rate of ALA into DHA.

195 ts of supplemental EPA can be converted into DHA.

196 iched with some essential nutrients (Inulin, DHA & EPA, vitamins B6, K1, and D3) as enhancers of calc

197 also yielded higher (p < 0.05) fillet lipid, DHA, and protein content (but not significantly differen

198 d that dietary lysophosphatidylcholine (LPC)-DHA significantly increases brain DHA, which results in

199 pholipid form called lysophosphatidylcholine DHA (DHA-lysoPC).

200 ere unrelated to outcomes, although maternal DHA at enrollment was related to productive vocabulary a

201 Mechanistically, DHA did not directly target B cells to elevate Ab levels

202 mice as lysophosphatidylcholine (LPC) (40 mg DHA/kg) for 30 days increased DHA content of the brain b

203 Participants took daily 465 mg DHA plus 600 IU vitamin E (DE), 465 mg DHA plus placebo

204 65 mg DHA plus 600 IU vitamin E (DE), 465 mg DHA plus placebo (DP), 600 IU vitamin E plus placebo (EP

205 and brain accumulation of the nanocarriers, DHA was more effective (P < 0.05) for improving BBB perm

206 whether DHA is metabolized to nonesterified DHA (free DHA) or a phospholipid form called lysophospha

207 brain mediated the physiological actions of DHA.

208 Here we show that oral administration of DHA to normal adult mice as lysophosphatidylcholine (LPC

209 At amounts of DHA in infant formula up to ~0.64%, AA contents should a

210 de range using different dietary carriers of DHA, and the correlations between the increase in brain

211 Comparison of DHA incorporation and Tf-receptor targeting showed that

212 signed to oral capsules providing 1.2 g/d of DHA from randomization to 36 weeks' postmenstrual age an

213 l trial, mothers received either 600 mg/d of DHA or a placebo beginning at 14.5 weeks of gestation an

214 ncept study has supported the development of DHA-based nanoARVs as an effective, safe yet technically

215 olid lipid nanoparticle (SLN) dispersions of DHA, were first produced by high-pressure homogenization

216 Screens performed under high doses of DHA provide evidence that mitochondrial metabolism can m

217 he role of His-50, we analyzed the effect of DHA on aS-derived species: a naturally occurring variant

218 this study was to investigate the effects of DHA (22:6n-3), vitamin E, and their probable interaction

219 have been explored for the encapsulation of DHA in the pH dependant polymer hydroxyl-propyl-methyl-c

220 viously reported decrease in the fraction of DHA-containing phospholipids and a compensatory increase

221 udies should evaluate the optimal intakes of DHA and AA in infants at different ages based on relevan

222 Levels of DHA-derived epoxides are lower in colon tissues from pat

223 provide a means to increase plasma levels of DHA-lysoPC, thereby decreasing the risk of AD.

224 as implemented for the microencapsulation of DHA/HPMCAS organic solutions, whilst in the second appro

225 aired brain transport of free DHA but not of DHA-lysoPC, as a consequence of a breakdown in the outer

226 neurones was also reduced in the presence of DHA.

227 ead to increased survival in the presence of DHA.

228 sulted in significantly higher quantities of DHA being encapsulated, at 2.09 g/100 g compared to 0.60

229 has been demonstrated that a major route of DHA entry in the retina is the delivery across the blood

230 taining the lysophosphatidylcholine route of DHA supply to the retina is essential for long-term phot

231 Dietary sources of DHA in phospholipid form may provide a means to increase

232 Release studies of DHA in the direct sprayed dried samples revealed a lag t

233 questioned whether the impaired synthesis of DHA affected neural plasticity and inflammatory status i

234 o review the state of scientific research on DHA and AA, and to discuss the questions arising from th

235 eir ability to synthesize DHA and survive on DHA-deficient diets.

236 m malaria were assigned treatment with AL or DHA-PQ and followed for 42 days.

237 ) cells were cultured with or without EPA or DHA (6.25-25 mug/mL) in the presence or absence of 0.5 m

238 an" AND "dihydroartemisinin-piperaquine" OR "DHA-PPQ".

239 We first confirmed that PEDF + DHA increased nerve regeneration in the mouse cornea.

240 right eye and treated in both eyes with PEDF+DHA for 2 weeks, there was a significant increase in cor

241 Role of phosphatidylcholine-DHA in preventing APOE4-associated Alzheimer's disease.

242 methylbutyrate (HMB), lutein, phospholipids, DHA and selected micronutrients including B12 and folic

243 ine (AL) and dihydroartemisinin-piperaquine (DHA-PQ) showed excellent treatment efficacy for uncompli

244 n, EPA supplementation did not change plasma DHA concentrations (P > 0.05) but did increase plasma de

245 AC, 5AC and zebularine) were the most potent DHAs and increased the enzymatic activity of SIRT6 witho

246 Although prenatal DHA supplementation substantially reduced early preterm

247 a few positive long-term effects of prenatal DHA supplementation emerged from analyses of this follow

248 p of infants from mothers receiving prenatal DHA supplementation in a US cohort.

249 teins, we show that the presence of the PUFA DHA helps helical multi-pass proteins such as GPCRs part

250 uld be explained by a combination of reduced DHA supply to the retina and a concomitant upregulation

251 In vivo, CAGE reduces DHA absorption by 60% to 70% compared with controls.

252 Reintroducing DHA in the diet of Elovl2(-/-) mice reversed such altera

253 N-S-LYS and N-S-DHA pups had a less permeable mucus barrier relative to

254 ozyme (N-S-LYS) or docosahexaenoic acid (N-S-DHA).

255 CA did not differ between high- and standard-DHA groups [wheeze: RR: 1.10; 95% CI: 0.73, 1.65; P = 0.

256 high-DHA (~1% total fatty acids) or standard-DHA (~0.3% total fatty acids) enteral feeds from 2-4 d o

257 station with high-DHA compared with standard-DHA enteral feeds decreases the incidence and severity o

258 Substituting DHA with another oil noticeably reduced the cellular upt

259 towards C24 PUFA enabling them to synthesise DHA through the Sprecher pathway.

260 leback increased their ability to synthesize DHA and survive on DHA-deficient diets.

261 Hence, impairment of systemic DHA synthesis can modify the brain inflammatory and neur

262 eover, 19,20-DHDP may be more effective than DHA as a nutritional supplement for preventing retinopat

263 EPA was more efficient than DHA in reducing production of arachidonic acid-derived l

264 It has long been believed that DHA supplementation increases plasma EPA via the retroco

265 In rodent contusion SCI, we demonstrate that DHA (500 nmol/kg) administered acutely post-injury confe

266 In parallel, we also found that DHA-deficient mice were characterized by an increased ex

267 Given that DHA metabolism by cytochrome P450 and soluble epoxide hy

268 These findings show that DHA induces neuroprotection in contusion injury.

269 n of the two FFA4 isoforms, and we show that DHA-mediated phosphorylation of FFA4-L is primarily regu

270 Comparative studies suggest that DHA may have stronger serum triglyceride-lowering effect

271 plasticity status, supporting the view that DHA is an essential fatty acid with an important role in

272 The DHA should equal at least the mean content in human milk

273 The DHA stability increased with the direct spray-drying app

274 descent infections were uncommon in both the DHA-PQ and AL arms (1.1% and 2.2%, respectively; P = .25

275 0.64%, AA contents should at least equal the DHA contents.

276 tion occurred in 53.2% of the infants in the DHA group and in 49.7% of the infants in the control gro

277 ificant pre-post clinical improvement in the DHA group versus placebo, using the Scale for the Assess

278 Mortality occurred in 6.0% of infants in the DHA group vs 10.2% of infants in the placebo group (abso

279 Overall, 147 of 268 infants (54.9%) in the DHA group vs 157 of 255 infants (61.6%) in the placebo g

280 ccurred in 41.7% of surviving infants in the DHA group vs 31.4% in the placebo group (absolute differ

281 n addition to a predictable reduction in the DHA level, the affected retinas undergo a complex, trans

282 ition of sEH and decreased generation of the DHA-derived diol 19,20-dihydroxydocosapentaenoic acid (1

283 n showed reduced leukocyte production of the DHA-derived monohydroxy fatty acid 17-hydroxy-DHA (HDHA)

284 miR-124 inhibitor significantly reduced the DHA-induced decrease in myelin phagocytosis in mice at 7

285 APOE4 carriers respond well to the DHA present in fish but do not respond as well to dietar

286 nt increase in the rate constant compared to DHA, even though the substrates have the same pK(a)(C-H)

287 Indeed, early studies using DHA dietary restriction documented reduced light sensiti

288 by an open-label study with overall 40-week DHA treatment.

289 roduction of proinflammatory lipids, whereas DHA abrogated the migration of Langerhans cells, as asse

290 strial origin lecithins (HL and SL), whereas DHA and EPA, a valuable omega-3 fatty acid, were the maj

291 This influences whether DHA is metabolized to nonesterified DHA (free DHA) or a

292 Moreover, aS forms a covalent adduct with DHA.

293 ommend that AA should be provided along with DHA.

294 fish intake were positively associated with DHA and the "high n-3 PUFA" pattern.

295 The association of cognitive benefit with DHA supplementation in predementia but not AD dementia s

296 h FVC when incorporating an interaction with DHA, and the finding was replicated (P(2df) = 9.4 x 10(-

297 risk of recurrent parasitemia was lower with DHA-PQ as compared to AL at all 3 sites at 42 days (26.0

298 )), was also prepared; for the reaction with DHA, an inverse KIE (compared to F(8)Cmpd-II(LutH(+))) w

299 in a microglia cell line (BV2) treated with DHA, and the effect was blocked by a miR-124 inhibitor.

300 Combined treatment with DHA and Physcion activates AMP-activated protein kinase,