ライフサイエンスコーパス: MDA

1 MDA and especially starch contents, were affected by chi

2 MDA has a small effect on reduction of MFI-BG.

3 MDA have indicated elevated levels and a decrease of GSH

4 MDA reduced malaria infection and clinical disease durin

5 MDA to only children 1-5 months old would avert ~186,000

6 MDA was conducted in 4 villages in Kayin State (Myanmar)

7 MDA, uric acid and ALT levels also increased, whereas GS

8 MDA-7/IL-24-mediated regulation of DICER is reactive oxy

9 MDA-MB231 and SKBR3 breast cancer cells grown in 3D down

10 expression of human myoglobin in MDA-MB-231, MDA-MB-468, and MCF7 breast cancer cells induces mitocho

11 of $4.89/DALY averted (95% UI: 2.88-11.42), MDA to all under-5 children would avert ~267,000 deaths

12 ort three different cell lines (i.e., MCF-7, MDA-231, and human-induced pluripotent stem-cell-derived

13 sheep red blood cells), cancer cells (MCF-7, MDA-435 and CD34(+)), yeast cells (saccharomyces cerevis

14 olites inside LECs in co-culture with MCF-7, MDA-MB-231, and SK-BR-3 breast cancer cell lines using [

15 ined from single cell platforms relying on a MDA-like amplification step, such as Chromium Single Cel

16 In highly mobile populations, accelerating MDA implementation increases likelihood of elimination;

17 stment in both the mass drug administration (MDA) and morbidity management programs, and this paper a

18 based on targeted mass drug administration (MDA) and, in 2017, on supplemental snail control.

19 to assess biannual mass drug administration (MDA) applied alone or with complementary snail control o

20 een distributed in mass drug administration (MDA) campaigns globally over the past 30 years.

21 ntation details of mass drug administration (MDA) campaigns.

22 re based on either mass drug administration (MDA) for LF, or insecticide-based interventions.

23 ion of large-scale mass drug administration (MDA) for neglected tropical diseases (NTDs).

24 d after ivermectin mass drug administration (MDA) for scabies in the Solomon Islands.

25 ty of infection to mass drug administration (MDA) for schistosomiasis.

26 ating azithromycin mass drug administration (MDA) for trachoma control has been confirmed by a recent

27 limination through mass drug administration (MDA) is hampered by coendemicity of Loa loa, as people w

28 ve of mass antimalarial drug administration (MDA) is to eliminate malaria rapidly by eliminating the

29 Mass drug administration (MDA) may further reduce malaria transmission in low-tran

30 Trials of mass drug administration (MDA) of azithromycin (AZM) report reductions in child mo

31 Ivermectin based mass drug administration (MDA) reduces the prevalence of scabies and, to a lesser

32 f treatment during mass drug administration (MDA) to control neglected tropical diseases.

33 F) and discontinue mass drug administration (MDA) with oral azithromycin.

34 Mass drug administration (MDA), the presumptive antimalarial treatment of an entir

35 ether azithromycin mass drug administration (MDA), the recommended antibiotic treatment strategy for

36 pecially following Mass Drug Administration (MDA), which is critical to understanding serostatus in t

37 to this problem is mass drug administration (MDA), with success depending on adequate population part

38 At 24 hours after administration, MDA-MB-231 or MCF-7 human breast cancer cells expressing

39 em, two rounds of mass drug administrations (MDAs) per year over two years (phase I, August 2015-2017

40 eroprevalence was 9.3% before and 5.1% after MDA (P = .019), demonstrating collateral benefits of ive

41 followed at baseline and for 6 months after MDA.

42 uming the survey was conducted 4 years after MDA.

43 eness of MDA to children 1-59 months of age, MDA to children 1-5 months of age, AZM administered at h

44 ntel plus 6 monthly single-dose albendazole) MDA.

45 e left kidney biochemical (malonyl-aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosi

46 ing and multiple displacement amplification (MDA) is widely used owing to its low error rate and long

47 we used multiple-displacement amplification (MDA) of cellular DNA diluted to a proviral endpoint to o

48 isplayed an increase in colonic IL-1beta and MDA, and a reduction of occludin at week 2.

49 nd non-CSC after treatment of MDA-MB-231 and MDA-MB-453 triple-negative breast cancer cells with a ne

50 D) suppressed tumor growth of MDA-MB-231 and MDA-MB-468 TNBC cells and spontaneous metastasis of MDA-

51 Overexpression of NMEs in MDA-MB-231T and MDA-MB-435 cancer cell lines increased endocytosis of tr

52 ed and mistaken for total FGF7 in SKBR-3 and MDA-MB-231 cells.

53 types of breast cancer xenografts (KPL-4 and MDA-MB-468).

54 Single cells from the core of 4T1 and MDA-MB-231 tumors grafts took up 26% to 84% less FDG tha

55 nt of the breast cancer cell lines MCF-7 and MDA-MB-231 and of breast epithelial cells MCF-10A with B

56 tted from (223)Ra in bone for both MCF-7 and MDA-MB-231 cells.

57 uman cell lines (GM12878, MCF-10A, MCF-7 and MDA-MB-231).

58 ells representing malignant (MCF-7 cells and MDA-MB-231 cells) and nonmalignant (MCF-10A cells) state

59 wo highly motile TNBC cell lines (Hs578T and MDA-MB-231) to provide a repository of signaling determi

60 3 and 113 migratory modulators of Hs578T and MDA-MB-231, respectively, which are linked to signaling

61 enced the levels of ALP, AMY, GLOB, IgM, and MDA (P < 0.05).

62 and invasion activities of T-DM1R-JIMT1, and MDA-MB-231 and BT-549 cells are regulated by different m

63 treated with 2-HOBA have reduced MDA-LDL and MDA-HDL levels, and their HDL display increased capacity

64 t cancer with different malignancy (MCF7 and MDA-MB 231).

65 determine their effect on growth in MCF7 and MDA-MB-486 cells.

66 humans determined by ultrasensitive PCR, and MDA was characterized by generalized estimating equation

67 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mut

68 Annual MDA could be followed by focal MDA targeting individuals

69 from before MDA and after 2 rounds of annual MDA from Kenya and Tanzania.

70 Both IgM anti-PC and anti-MDA increased during the first 2 y of life, but IgM anti

71 For anti-MDA, preprogramming is likely to play a major role and a

72 vels as mothers' after 2 y, whereas IgG anti-MDA reached similar levels as mothers' already after 1 y

73 low levels of IgM anti-PC, whereas IgM anti-MDA was present at birth.

74 ife, but IgM anti-PC in contrast to IgM anti-MDA was still significantly lower than in the mothers.

75 ti-PC) and Abs against malondialdehyde (anti-MDA) may be protective in chronic inflammation, like ath

76 anti-PC levels develop much slower than anti-MDA and are still relatively low at 2 y.

77 rting the conclusion that further antibiotic MDA is not currently required for trachoma elimination p

78 axel in A549 non-small cell lung, as well as MDA-MB-436 and SUM149 triple negative breast cancer xeno

79 effectors, YT cells loaded with GrB attacked MDA-MB-231 target cells, and active GrB influenced its t

80 ulation-level implementation of azithromycin MDA may lead to selection of multiresistant pathogens.

81 hroughout any implementation of azithromycin MDA, focusing on a genotypic approach to overcome the li

82 Evidence suggests that repeated azithromycin MDA may result in a sustained increase in macrolide and

83 Intensive community-based MDA has a limited impact in high-schistosomiasis-transmi

84 her ivermectin-based MDA or ivermectin-based MDA co-administered with azithromycin.

85 andomized to receive either ivermectin-based MDA or ivermectin-based MDA co-administered with azithro

86 Mice bearing MDA-MB-231 breast cancer and FaDu head neck cancer xenog

87 predictive approaches using data from before MDA and after 2 rounds of annual MDA from Kenya and Tanz

88 Individuals infected before MDA had a 2-fold higher odds of reinfection post-MDA (ad

89 receive one of three interventions: biannual MDA with praziquantel alone (arm 1) or in combination wi

90 hat modify the ability of plasma CFH to bind MDA in 1,830 individuals and characterized the mechanist

91 uoroamphetamine and two ring-isomers of both MDA and MDMA, we demonstrate the ability of IRIS to dist

92 mice bearing human brain (U251) and breast (MDA-MB-468) tumor xenografts treated with a single dose

93 al cells, obtained in vitro and amplified by MDA.

94 Plasmodium vivax infections were cleared by MDA.

95 NAs was transfected into human breast cancer MDA-MB-231 cells.

96 a GL261, human triple negative breast cancer MDA-MB-231, human pancreatic cancer MIAPaCa-2, and human

97 er (HT29) and AQP1-expressing breast cancer (MDA), and low-AQP1-expressing SW480.

98 Breast cancer (MDA-MB-231) and liver cancer (HepG2) cell lines were als

99 tastatic colon [HT29(US)] and breast cancer (MDA-MB-231) cell lines.

100 DNA-binding activity in human breast cancer, MDA-MB-231 or MDA-MB-468 cells.

101 r concordance (kappa value) for Evans', CAP, MDA, JPS and ART grading systems were 0.34, 0.50, 0.65,

102 en-resistant MCF-7, mouse mammary carcinoma, MDA-MB-231, and BT-549) viability, migration, and bindin

103 ic adenocarcinoma, OvCar3 ovarian carcinoma, MDA-MB-231 breast adenocarcinoma, and HL-60 promyelocyti

104 on, we here investigated breast cancer cell (MDA-MB-231) migration by video microscopy as a function

105 y in the triple-negative breast cancer cells MDA-MB-231.

106 in cells without actin cap: cancerous cells MDA-MB-231, which naturally lack the actin cap, and NIH

107 take in triple negative breast cancer cells (MDA-MB-231).

108 he dynamics of human breast carcinoma cells (MDA-MB-231) in these microstructures as a function of ar

109 ly, GPX8 knockout in mesenchymal-like cells (MDA-MB-231) resulted in an epithelial-like morphology, d

110 te that culturing tumor spheroids containing MDA-MB-231 cells + HUVECs in an HLF-laden, fibrin-based

111 , but will not benefit much from the current MDA program, which is aimed at reducing transmission.

112 r the course of 58 days (KPL-4) and 16 days (MDA-MB-468), and the evolution of functional vasculature

113 O1-proficient A549 tumors and NQO1-deficient MDA-MB-231 tumors were developed in the same animal, onl

114 zes the direct methane dehydroaromatization (MDA) best so far is Mo supported on zeolite.

115 insights about methane dehydroaromatization (MDA) to benzene over ZSM-5-supported transition metal ox

116 ically-limited Methane DehydroAromatization (MDA) to benzene under non-oxidative conditions appears v

117 -kB, CREB and AP-1 activation in DeltaMEGF11 MDA-MB-231 and 468 cells.

118 ch the control villages received deferred DP MDA.

119 irs to select 8 villages to receive early DP MDA and 8 villages as controls for 12 months, after whic

120 ria control measures, 3 monthly rounds of DP MDA reduced the incidence and prevalence of falciparum m

121 and well-resourced elimination programme, DP MDA can be a useful additional tool to accelerate malari

122 The DP MDAs were well tolerated; 6 severe adverse events were d

123 es) received ivermectin inadvertently during MDA campaigns in the observational studies and 397 pregn

124 (x) sites, nature of the active sites during MDA, reaction mechanisms, rate-determining step, kinetic

125 sis supports an association between elevated MDA-9 and bone metastasis and poor prognosis.

126 lines and clinical samples display elevated MDA-9 expression and bioinformatic analysis supports an

127 onstrated specific uptake in CD44-expressing MDA-MB-231 tumors.

128 Annual MDA could be followed by focal MDA targeting individuals infected during the dry season

129 Seroconversion rates were lower following MDA and seroreversion rates were slightly higher compare

130 of these seroreverted to negative following MDA.

131 This finding has important implications for MDA programme effectiveness, the relevance of which will

132 hypoendemic areas currently not targeted for MDA.

133 that tested a lower-prevalence threshold for MDA and shorter intervals between implementation, evalua

134 tional significance, treatment of pre-formed MDA(w)-tumors with a lentiviral-TRAF3IP2-shRNA not only

135 The four MDA rounds covered 58%-72% of the population, and annual

136 ive pharmacovigilance system during the four MDA rounds.

137 an isogenic panel of cell lines derived from MDA-MB-231 breast cancer cells that vary in their metast

138 Two cell lines derived from MDA-MB-231 breast cancer cells were transfected with the

139 el of human breast cancer cells derived from MDA-MB-231 cells.

140 d progression of advanced BC metastasis from MDA-MB-231 BC cells in bones and lungs of nude mice.

141 ther, the M.D. Anderson Cancer Center group (MDA) and the Japan Pancreas Society (JPS) have introduce

142 ceptor expression and MMP activity (HT1080 > MDA-MB-231 > B8484 > MCF7).

143 tivity on different tumor cell lines (HepG2, MDA-MB-231, MCF-7 and Caco2).

144 ancer cells that express low levels of HER2 (MDA-MB-231 and BT-549 cells).

145 ICER in cancer cells impedes Ad.mda-7 or His-MDA-7/IL-24 inhibition of cell growth, colony formation,

146 activity in a panel of cancer cells (HT1080, MDA-MB-231, B8484, and MCF7).

147 oth syngeneic murine 4T1 and xenograft human MDA-MB-231 breast cancer models.

148 We identify MDA-9 as a key contributor to NB pathogenesis and show t

149 In MDA-MB-231-derived human triple-negative breast cancer c

150 tion after the transfection of miR-19b-3p in MDA-MB-231 cells.

151 ing levels of NAT1 N-acetylation activity in MDA-MB-231 breast cancer cells on global cellular metabo

152 assays and increased caspase 3/7 activity in MDA-MB-231 cells in comparison to cells treated with DTX

153 l EMT or mesenchymal-like carcinoma cells in MDA-MB-468 tumors treated with the paclitaxel-nilotinib

154 suggested to be inhibition of HS cleavage in MDA-MB-231 triple-negative breast cancer (TNBC) cells.

155 xygen species (ROS) to inflict cell death in MDA-MB-231 cells, demonstrating the potency of this trea

156 sion and cell migration were demonstrated in MDA-MB-231 cells.

157 DA(w)-injected animals, none was detected in MDA(KDRab27a)- or MDA(KDTRAF3IP2)-injected animals.

158 While metastasis was detected in MDA(w)-injected animals, none was detected in MDA(KDRab2

159 ve GAPDH inhibitor, caused about 70% drop in MDA-MB-231 cell viability at 20 muM while 40 muM IA was

160 nockdown (DeltaMEGF11) or over-expression in MDA-MB-231 and MB-468 cells, cell growth and chemokine g

161 ed to an increase in Claudin-1 expression in MDA-MB-231 cells, while ADAM15B had no effect.

162 e images for cytoplasmic and nuclear FGF7 in MDA-MB-231 cells were duplicated and mistaken for total

163 d selective accumulation of (111)In-PA-L1 in MDA-MB-231 tumor xenografts (5.7 +/- 0.9 percentage inje

164 ng the EGF-EGFR signaling axis as a model in MDA-MB-231T cells, NME1 decreased pEGFR and pAkt express

165 vitro that expression of human myoglobin in MDA-MB-231, MDA-MB-468, and MCF7 breast cancer cells ind

166 Overexpression of WT NCS1 in MDA-MB231 breast cancer cells increased Ca(2+) signaling

167 axel with the BCR-ABL inhibitor nilotinib in MDA-MB-468 breast cancer xenografts) caused changes in t

168 Overexpression of NMEs in MDA-MB-231T and MDA-MB-435 cancer cell lines increased e

169 P. falciparum infections who participated in MDA and could be followed up, 207 (94%) cleared their in

170 pression only on both cell subpopulations in MDA-MB-231 cell line.

171 We also demonstrated that in MDA-MB-231 breast cancer cells, the cell-surface transpo

172 However, the phi29 polymerase used in MDA is sensitive to template fragmentation and presence

173 eries, FCW34 and FCW66 were shown to inhibit MDA-MB-231 cell migration as effectively as ST3GALIII-ge

174 rther evaluation of the safety of integrated MDA for NTDs.Clinical Trials Registration.

175 Intensive MDA reduced Schistosoma mansoni infection intensity: the

176 Ca2+-dependent and is required for invasive MDA-MB-231 cell migration as well as for gelatin degrada

177 onstrating collateral benefits of ivermectin MDA in this setting.

178 ion in accordance with the CAP, Evans', JPS, MDA and ART grading systems, and interobserver concordan

179 ly suppress metastasis in the DNM2 knockdown MDA-MB-231T cells.

180 s of oxidized LDL (oxLDL), MDA-modified LDL (MDA-LDL), and advanced glycosylation-modified LDL (AGE-L

181 Conversely, in a breast cancer cell line MDA-MB-231 NMDAR blockade results in an increase in endo

182 e invasively growing breast cancer cell line MDA-MB-231 requires high concentrations of CUR for tumor

183 at in the metastatic breast cancer cell line MDA-MB-231, retromer regulates the matrix invasion activ

184 carcinoma cell line HepG2 and the TNBC line MDA-MB-231.

185 ing triple-negative breast cancer cell line (MDA-MB-231-luc) were treated with varying concentrations

186 CSF1, miR-149 expression in TNBC cell lines (MDA-MB-231 and BT-549) inhibited the recruitment of huma

187 sion changes of three metastatic cell lines (MDA-MB-231, A549, T24) in 2D versus 3D environments.

188 h STAT3-proficient breast cancer cell lines (MDA-MB-231, SUM149) revealed that Stattic attenuated his

189 P1-mCherry, a marker for DNA damage, in live MDA-MB-231 cells.

190 and plant extracts was associated with lower MDA levels and MetMb percentage and higher levels of vit

191 kPa, G (l) = 4.7 +/- 0.2 kPa, n = 7) and luc-MDA-MB-231-LM2-4 (G (d) = 7.9 +/- 0.4 kPa, G (l) = 6.0 +

192 ma xenografts, intracranially propagated luc-MDA-MB-231-LM2-4 (G (d) = 3.7 +/- 0.2 kPa, G (l) = 2.2 +

193 compared to wild type albumin, in luciferase MDA-MB-231-Luc-D3H2LN breast cancer xenografts was shown

194 ation of hydroperoxides and malondialdehyde (MDA) compounds.

195 eukin (IL)-1beta, IL-6, and malondialdehyde (MDA) levels were measured.

196 solevuglandins (IsoLGs) and malondialdehyde (MDA) that covalently modify proteins.

197 nd fast method to determine malondialdehyde (MDA) levels in raw and processed meat.

198 ile significantly enhancing malondialdehyde (MDA), H(2)O(2), electrolyte leakage, oxidized glutathion

199 ls of lipid hydroperoxides, malondialdehyde (MDA) and 4-hydroxy-trans2-hexenal (HHE) in both herring

200 , a significant increase in malondialdehyde (MDA) production and a decrease in biofilm formation and

201 (ROS) scavenging including malondialdehyde (MDA) as a measure of lipid peroxidation, ascorbate, tota

202 ve stress markers including malondialdehyde (MDA), advanced protein oxidation product (APOP), myelope

203 ss i) increased post-mortem malondialdehyde (MDA) formation except in vacuum-stored meat, ii) decreas

204 The formation of malondialdehyde (MDA), 4-hydroxy-2-hexenal (HHE), 4-hydroxy-2-nonenal (HN

205 Cardiac tissue levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), cat

206 and biochemical parameters (Malondialdehyde (MDA) and starch content) from the pericarp or columella.

207 TVBN), peroxide value (PV), malondialdehyde (MDA), and bacteria levels.

208 altered self-ligands (e.g., malondialdehyde [MDA]-modified molecules) involved in homeostasis, thereb

209 e (ALAT); oxidative stress (malondialdehyde [MDA], reduced glutathione/oxidative glutathione ratio [G

210 d from three breast cancer cell lines (MCF7, MDA-MB-231 and SKBR3).

211 6%) cells, but not for the highly metastatic MDA-MB-231 cell.

212 ock-down experiments on the highly migratory MDA-MB-231 cell lines and deriving gene knock-down based

213 Methods: ER-negative MDA-MB-231 breast cancer cells were used to generate sta

214 body inhibited the growth of triple negative MDA-MB-231 tumors to a greater extent in nude mice than

215 RAF3IP2 (MDA(KDTRAF3IP2)) in triple negative MDA-MB231 cells reduced tumor growth by 70-97% compared

216 < 0.001) and invasiveness of triple-negative MDA-MB-231 cells (p < 0.001).

217 rates in this same cohort in the absence of MDA.

218 Importantly, the invasion activity of MDA-MB-231 and BT-549 cells is also significantly increa

219 Immunofluorescence analysis of MDA-MB-231 ADAM15A expressing cells showed Claudin-1 at

220 t hospital discharge, and the combination of MDA and post-discharge AZM.

221 The concentration of MDA was similar for most of the matrices in both UPLC me

222 cell lines while GD3 was decreased in CSC of MDA-MB-231 cell line.

223 detected to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be signi

224 gram cycle that initiated discontinuation of MDA (TF1-9 prevalence <5%), followed by a surveillance s

225 5% threshold, warranting discontinuation of MDA.

226 We evaluated the effect of MDA discontinuation on TF1-9 prevalence at the district

227 es did not significantly boost the effect of MDA in our study, they might enhance interruption of tra

228 We modeled the cost-effectiveness of MDA to children 1-59 months of age, MDA to children 1-5

229 nd shrimp by-product mitigated generation of MDA and HHE in herring PI.

230 lly exposed to T-DM1 although cell growth of MDA-MB-231 and BT-549 cells is not inhibited by T-DM1.

231 ry of miR-127(PD) suppressed tumor growth of MDA-MB-231 and MDA-MB-468 TNBC cells and spontaneous met

232 capture the particle uptake heterogeneity of MDA-MB-231 cells.

233 We uncover how the impact of MDA campaigns is determined by the interaction between i

234 2015 and 2025, accounting for the impact of MDA with ivermectin.

235 forces, cell morphology, and invasiveness of MDA-MB 231 breast cancer cells in three-dimensional coll

236 To understand the mechanism of MDA-MB-231 cell survival, we studied metabolic modulatio

237 468 TNBC cells and spontaneous metastasis of MDA-MB-231 cells.

238 ny cytotoxicity in vitro in 2D monolayers of MDA-MB-231 (triple negative breast cancer), MCF7 (breast

239 was not treated during the previous round of MDA (adjusted odds ratio [OR] 3.60, 95% CI 3.08-4.20 for

240 Annual rounds of MDA with dihydroartemisinin-piperaquine (DP) were implem

241 In a study with multiple rounds of MDA, data collected before the third MDA were used to pr

242 ls not being treated over multiple rounds of MDA, which we term systematic non-treatment.

243 ession on CSC and non-CSC after treatment of MDA-MB-231 and MDA-MB-453 triple-negative breast cancer

244 , before initiating or after 1 or 2 years of MDA could help guide programmatic decision making.

245 inhibiting alternative pathway activation on MDA-modified surfaces, we performed an unbiased genome-w

246 CFH from mediating its cofactor activity on MDA-modified surfaces, resulting in enhanced complement

247 lectrical pulses (EP) and Cisplatin (CsP) on MDA-MB-231, human TNBC cells.

248 phy-tandem mass spectrometry (UPLC-MS/MS) on MDA-MB-231 breast cancer cell lines constructed with siR

249 tivity in human breast cancer, MDA-MB-231 or MDA-MB-468 cells.

250 mals, none was detected in MDA(KDRab27a)- or MDA(KDTRAF3IP2)-injected animals.

251 Mice bearing orthotopic MDA-MB-231 breast cancer xenografts were imaged noninvas

252 , lung metastases developing from orthotopic MDA-MB-231 tumors were reduced by 75% by miR-149 express

253 the baseline levels of oxidized LDL (oxLDL), MDA-modified LDL (MDA-LDL), and advanced glycosylation-m

254 , and bone marrow, all derived from parental MDA-MB-231 triple-negative breast cancer cells.

255 in the case of the most malignant phenotype (MDA-MB-231).

256 ence declined in the first three months post-MDA.

257 had a 2-fold higher odds of reinfection post-MDA (adjusted odds ratio = 2.5, 95% confidence interval

258 isease, and risk of malaria reinfection post-MDA were determined.

259 Knockdown (KD) of Rab27a (MDA(KDRab27a)) or TRAF3IP2 (MDA(KDTRAF3IP2)) in triple n

260 r(-/-) mice treated with 2-HOBA have reduced MDA-LDL and MDA-HDL levels, and their HDL display increa

261 d effect of TurNP + EP treatment in reducing MDA-MB-231 cell viability to as low as 9% at 12 h.

262 ying the composition of the tumor spheroids (MDA-MB-231 breast tumor cells + mesenchymal stem cells (

263 (TNF-alpha and IL-1beta), oxidative stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that

264 We also show that MDA-MB-231 cell lysates can "seed" aggregation of the ce

265 The MDA comprised 3 monthly rounds of 3 daily doses of DP an

266 ng the catalytic sites before and during the MDA reaction.

267 The findings from the MDA catalysis literature is critically analyzed with emp

268 hat addition of culture supernatant from the MDA-MB-134-VI FGFR-amplified breast cancer cells-activat

269 ly, micrometastasis was detected only in the MDA(KDRab27a)-injected group.

270 icancer activity by growth inhibition in the MDA-MB-231 breast cancer cell line and low IC(50) (225.1

271 drug combination (Olaparib + BKM120) in the MDA-MB-468 xenograft model with a tumor growth inhibitor

272 step, kinetics and catalyst activity of the MDA reaction.

273 Importantly, 2-HOBA reduces the MDA- and IsoLG-lysyl content in atherosclerotic aortas v

274 Results: The MDA-MB-231 xenografts were observed to have a 10-day gro

275 Prior to the MDA program, approximately 129 million people were infec

276 Prior to the MDA programme approximately 129 million were infected wi

277 unds of MDA, data collected before the third MDA were used to predict PHS.

278 Thus, MDA-SGS can be used for "viral reconstruction" to better

279 e human triple negative breast cancer (TNBC, MDA-MB-231 cells) growing in the brains of athymic nude

280 HR1 and FHR3 compete with CFH for binding to MDA-epitopes and that FHR1 displays the highest affinity

281 ic variants that modify CFH/FHL-1 binding to MDA.

282 Moreover, FHR1 bound to MDA-rich areas on necrotic cells and prevented CFH from

283 e health and economic burdens of LF prior to MDA programs starting in GPELF areas.

284 at FHR1 displays the highest affinity toward MDA-epitopes compared to CFH and FHR3.

285 (KD) of Rab27a (MDA(KDRab27a)) or TRAF3IP2 (MDA(KDTRAF3IP2)) in triple negative MDA-MB231 cells redu

286 he device was used to enrich CoCl(2) treated MDA-MB 231 breast cancer cells from an untreated populat

287 ced by IL-4-polarized macrophages triggering MDA-MB-231 cell apoptosis in combination with SM-164.

288 ude mice bearing CD44-positive human tumors (MDA-MB-231, breast cancer, triple-negative).

289 owth by 70-97% compared to wild-type tumors (MDA(w)).

290 Using MDA-MB-231 breast cancer MCTS, we estimated biophysical

291 Using MDA-MB-468 and SUM-159PT TNBC cells, along with LC-MS/MS

292 Here we show, using MDA-MB-231 cells as a model, that the plasticity of at l

293 ges in Kenya, and then simulated control via MDA.

294 In-vivo studies, where MDA-MB-231 xenografts were exposed to necrotic lysates,

295 ocused on a time-limited intervention, while MDA implemented for mortality benefits would likely repe

296 assigned to receive biannual community-wide MDA for soil-transmitted helminthiasis to longitudinal r

297 ant Plasmodium falciparum is now widespread, MDA has been proposed as an elimination accelerator, but

298 Furthermore, in macrophages cocultured with MDA-MB-231 cells expressing miR-149, epidermal growth fa

299 n the study had infection, and coverage with MDA was 97%.

300 astatic burden in vivo in mice injected with MDA-MB-231 breast cancer cells.