ライフサイエンスコーパス: MCT

1 MCT and MCT+AP rats also developed pulmonary artery medi

2 MCT and MCT+AP rats developed PH with respective right v

3 MCT feeding stimulated jejunal-epithelial thymic stromal

4 MCT in the ES stroma were more degranulated than in thos

5 MCT of A. funestus switched from 2 AM in Lokohoue and 3

6 MCT oil consumption resulted in lower endpoint body weig

7 MCT suppressed antigen absorption into blood but stimula

8 MCT(sl/sl) rats developed more severe PAH, characterized

9 MCT-1 contains the PUA domain, a recently described RNA-

10 MCT-1 is an oncogene that was initially identified in a

11 MCT-1 protein is stabilized in response to DNA damage.

12 MCT-injected rats developed severe PH by day 21 and prog

13 MCT-sensitized mice experienced IgG-dependent anaphylaxi

14 line, multiple copies in T-cell lymphoma-1 (MCT-1), that has been shown to decrease cell-doubling ti

15 , we identify monocarboxylate transporter-1 (MCT-1) as a receptor used by HERV-T for attachment and i

16 OS (80% olive oil and 20% SO), or MOSF (30% MCTs, 25% olive oil, 30% SO, and 15% FO).

17 tion or at follow-up at 52 weeks (HIIT, 39%; MCT, 25%; RRE, 34%; P=0.16).

18 colysis (monocarboxylate transporter type 4 [MCT-4]), and angiogenesis (vascular endothelial growth f

19 n triglycerides (MCTs) and 50% SO], MSF (50% MCTs, 40% SO, and 10% fish oil (FO)], OS (80% olive oil

20 Several airway diseases exhibit abnormal MCT, including asthma, chronic bronchitis, and cystic fi

21 importance in the CNS, little is known about MCT expression and lactate function in the PNS.

22 rich Ringer, with and without niflumic acid (MCT inhibitor), acetazolamide (ACTZ, a CA inhibitor), 5-

23 An acute MCT with a comparable baseline was available in 71 of 82

24 The magnitude of increase in acute MCT above the threshold predicted by consensus equation

25 Analyses confirmed that a rise in acute MCT greater than that defined by the equation had a sens

26 2 mg/L) has been proposed to interpret acute MCT in mast cell activation syndrome (MCAS).

27 in a subgroup of participants (n = 16) after MCT supplementation.

28 ly and precipitously during 23-32 days after MCT.

29 and increased IL-4 and IL-13 secretion after MCT/EW challenge.

30 We evaluated an MCT-1 inhibitor, AS2495674, in a rat heart transplant mo

31 human mast cells were suppressed by LA in an MCT-dependent manner.

32 are always, sometimes, or never a part of an MCT.

33 27), HK-3 (P = 0.013), VEGF (P = 0.049), and MCT-4 (P = 0.020).

34 ession were observed for GLUT-1, GLUT-3, and MCT-4.

35 her agent alone, indicating that GABA(B) and MCT inhibitors, alone and in combination, represent pote

36 The operator's impact on CCT and MCT measurements is insignificant in all devices.

37 CCT and MCT measurements show moderate agreement between instrum

38 sight into mechanisms of PH caused by CH and MCT toxicity.

39 nto their respective groups (normal, CH, and MCT) but also to gain insight into mechanisms of PH caus

40 ence of oil phase composition (vitamin D and MCT), surfactant-to-oil ratio (SOR), surfactant type (Tw

41 12 weeks was not different between HIIT and MCT (P=0.45); left ventricular end-diastolic diameter ch

42 here was also no difference between HIIT and MCT in peak oxygen uptake (P=0.70), but both were superi

43 ion to their role in initiation, Ligatin and MCT-1/DENR can promote release of deacylated tRNA and mR

44 MCT and MCT+AP rats also developed pulmonary artery medial hyper

45 MCT and MCT+AP rats developed PH with respective right ventricul

46 Furthermore, MCT12 was identified as another MCT isoform that requires CD147 for trafficking to the c

47 ine decreased in the order LCT approximately MCT>>orange oil; whereas beta-carotene bioaccessibility

48 sodium lactate revealed that LA effects are MCT-1- and pH-dependent.

49 To assess MCT, we tracked movement of radiodense microdisks in air

50 e transporter (MCT) 2 but not the astrocytic MCTs (MCT1 and MCT4).

51 ol ELPCs (expressing nuRFP alone) attenuated MCT-induced right ventricular systolic pressure increase

52 tein into the oocyte cytosol did not augment MCT transport function.

53 he acidic milieu surrounding tumors, because MCT is increasingly active as extracellular pH decreases

54 However, there was no difference between MCT and the corn oil control supplement in the intestina

55 h a functional molecular interaction between MCT-1 and the MEK/ERK signaling pathway and suggest that

56 Both MCT and MCTC in tumour islets were higher in ES (20.0 an

57 Since both MCT and MCTC infiltrating tumour islets in ES NSCLC pati

58 s that was inhibited by niflumic acid and by MCT siRNA knockdown, and significantly reduced in the pr

59 , blocking TSP1 in the medium conditioned by MCT-1-negative cells restored its angiogenic potential t

60 Overall, the murine model of PH elicited by MCT mimics loss of body weight and diaphragm muscle weak

61 monary vascular remodeling and PH induced by MCT are different from those induced by CH.

62 However, it is unclear if PH induced by MCT in mice reproduces the loss of body weight and diaph

63 rmalities in a murine model of PH induced by MCT.

64 lic interactions are most likely mediated by MCTs.

65 lock ancHTenv mediated infection, by causing MCT-1 depletion from cell surfaces.

66 onstration of chemical sensing using on-chip MCT waveguides, monolithically fabricated IR sensing sys

67 Limitations of current MCT assays and of current animal models of human disease

68 bicarbonate transport, explaining defective MCT that occurs even in the presence of adequate PCL hyd

69 airway surface liquid contributes to delayed MCT beyond that caused by airway dehydration alone and i

70 Dietary MCTs promote allergic sensitization and anaphylaxis by a

71 We sought to test how dietary MCTs affect food allergy.

72 ell lymphomas (DLBCL) and that knocking down MCT-1 by a specific short hairpin RNA in DLBCL cells ind

73 mayonnaise remained intact containing either MCT oil or LSO.

74 Employing MCT-1 oncogene-mediated transformation of immortalized b

75 breast cancer cells negative for endogenous MCT-1 (MCF7-MCT-1).

76 Knockdown of endogenous MCT-1 using an siRNA approach attenuates the H2AX phosph

77 ation in kidney proximal tubular epithelial (MCT) cells.

78 pha-cyano-4-OH-cinnamate, a well established MCT inhibitor.

79 Normal airways compensate for MCT-driven H(+) secretion by secreting HCO3(-), a proces

80 and extent of lipid digestion was higher for MCT- than LCT-emulsions, which was attributed to differe

81 es apoptosis, supporting a critical role for MCT-1 in DLBCL cell survival.

82 Our data establish a role for MCT-1 in translational regulation, and support a linkage

83 Furthermore, MCT-1 is capable of transforming immortalized human mamm

84 impact of 4 wk of supplementation with 20 g MCT oil/d or 20 g corn oil/d on the kinetics of apolipop

85 As a result, we found that these glycolytic/MCT-deficient cells resumed growth by redirecting their

86 Group MCT targeting cognitive biases vs neuropsychological tra

87 mately fish oil > orange oil > mineral oil > MCT.

88 bioaccessibility decreased in the order LCT>>MCT>orange oil.

89 2 weeks of supervised interventions of HIIT, MCT, or a recommendation of regular exercise (RRE).

90 Expression of human MCT-1 in the Deltatma20 yeast mutant complemented transl

91 ased level of p63 transcript in hypertrophic MCT cells (an established cell model of chondrocyte matu

92 Impaired MCT was not due to periciliary liquid depletion; rather,

93 Thus, impaired MCT is a primary defect in CF, suggesting that submucosa

94 In MCT cells, a mouse renal proximal tubule cell line, ATP

95 In MCT cells, inhibition of gamma-secretase similarly atten

96 In MCT(sl/sl) rats, morphometric evaluation revealed the pr

97 nd was relatively low ( approximately 2%) in MCT nanoemulsions because the mixed micelles formed were

98 HIIT and -1.2 mm (-3.6 to 1.2 mm; P=0.34) in MCT.

99 hallenges of sensitized mice with antigen in MCT significantly aggravated anaphylaxis compared with c

100 tting were performed to determine changes in MCT expression after scratch wounding and re-epitheliali

101 The ability to quantify in vivo changes in MCT may have utility in pre-clinical research studies de

102 he aim of this study was to image changes in MCT produced by a rehydrating treatment based on hyperto

103 pression of ET(B) receptors was decreased in MCT(sl/sl) rat lungs, ET(A) receptor expression increase

104 in with MCT, as well as prolonged feeding in MCT-based diets, caused spontaneous allergic sensitizati

105 ES protocol, but there was no improvement in MCT performance.

106 dose of AE produced the most improvement in MCT with dose-dependent changes in Klotho in the blood.

107 d MCT4 resulted in a significant increase in MCT transport activity, even in the nominal absence of C

108 were statistically significant increases in MCT in the isotonic and HS-P308 groups.

109 H/HeJ mice were fed peanut butter protein in MCT, LCT (peanut oil), or LCT plus an inhibitor of chylo

110 a-tocopherol during storage being similar in MCT and LSO mayonnaises, but being stable in mixed oil m

111 ring supervised HIIT and 80% above target in MCT.

112 duced pulmonary preferential vasodilation in MCT induced PAH rats.

113 tes were down-regulated by AZD6244 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.

114 Inhibiting MCT-1 leads to long-term graft survival in rodent heart

115 tment with the 3-mAb cocktail during initial MCT/EW immunization induced EW tolerance.

116 itory molecule targeting ERK, we interrupted MCT-1 phosphorylation and stability.

117 We further investigated MCT as a potential therapeutic target in vitro.

118 inutes after injection of saline or 60 mg/kg MCT, rats were assigned to receive a daily injection of

119 MMP-9/TIMP-1 ratio, and significantly lower MCT-1 and CD98 levels, factors associated with EMMPRIN f

120 Multiple copies in T-cell maligancy (MCT-1) is a putative oncogene initially identified in a

121 In general, many MCTs exist for a given network; here we characterize a b

122 er cells negative for endogenous MCT-1 (MCF7-MCT-1).

123 its angiogenic potential to that of the MCF7-MCT-1 cells.

124 In a tumor xenograft model, MCT-1-overexpressing cells showed higher take rates and

125 pharmacological efficacy in a monocrotaline (MCT) induced rat model of PAH.

126 rmal chronic hypoxia (CH) and monocrotaline (MCT) models of pulmonary hypertension (PH), followed by

127 ts, hypoxia-exposed mice, and monocrotaline (MCT)-treated rats.

128 ys after transposon delivery, monocrotaline (MCT) was administered to induce PH.

129 peptide on the development of monocrotaline (MCT)-induced PH.

130 a single subcutaneous dose of monocrotaline (MCT, 60 mg/kg) to induce PH-associated RVF (PH, n=24) or

131 ng of lung and heart in a rat monocrotaline (MCT) model of pulmonary hypertension.

132 RFP) were tested in rats with monocrotaline (MCT)-induced PAH.

133 ts with pressure-induced RVF (monocrotaline [MCT] injection, n = 25; controls with saline injection,

134 model of PH induced by drug (monocrotaline, MCT) has been extensively used in mice to examine the et

135 nalogue of Northern methanocarbathymidine (N-MCT), 2 and 3, are reported.

136 We show that 2'-F incorporation on the N-MCT scaffold has a strong stabilizing effect on duplex t

137 In ES 44% of MCT and 37% of MCTC expressed TNFalpha in the tumour isl

138 g pathway and suggest that the activation of MCT-1 function by its upstream kinase ERK plays an impor

139 Therefore, we developed an in vivo assay of MCT, and here we describe its use in newborn wild-type p

140 CAIV-mediated augmentation of MCT activity was independent of the CAIV catalytic funct

141 d not suppress CAIV-mediated augmentation of MCT transport activity.

142 Consumption of MCT oil as part of a weight-loss plan improves weight lo

143 We aimed to determine whether consumption of MCT oil improves body weight and fat loss compared with

144 rkers to support the clinical development of MCT inhibitors now in clinical trials.

145 hows, for the first time, that disruption of MCT binding to their chaperon, Basigin, may be an effect

146 ASH was assessed, as well as the effects of MCT blocker and MCT2 antisense oligonucleotides and siRN

147 tential mechanisms underlying the effects of MCT on triglyceride-rich lipoprotein (TRL) metabolism ha

148 Forced expression of MCT-1 has recently been shown to induce cell transformat

149 Forced expression of MCT-1 significantly increases the number of DNA damage-i

150 er, our results suggest that facilitation of MCT transport activity by CAII requires direct binding b

151 The increased granularity of MCT data provided by this assay may provide an opportuni

152 In the hypertrophied hearts of MCT-treated rats, we found a significant increase in the

153 Understanding the impact of MCT blockade on tumor cell metabolism may help develop c

154 The impact of MCT-1 overexpression on DNA damage response remains unkn

155 Significantly, cells with distinct levels of MCT-1 protein displayed differential sensitivity to ERK

156 there were significantly increased levels of MCT-1 protein in a subset of primary diffuse large B-cel

157 Levels of MCT-1 protein were shown to be increased after exposure

158 ted malignancies that exhibit high levels of MCT-1 protein.

159 positive BMD cells engrafted in the lungs of MCT-treated rats.

160 investigate the ultrastructural mechanics of MCT by measuring fibril strain at different chemically i

161 However, the mechanisms of MCT have not been characterized at the nanoscale.

162 Understanding the mechanisms of MCT quantitatively may have applications in development

163 ped to explain the biophysical mechanisms of MCT.

164 he right ventricle revealed that a number of MCT-altered genes and neurotransmitter pathways (dopamin

165 ches, we established that phosphorylation of MCT-1 protein by p44/p42 mitogen-activated protein kinas

166 In the presence of MCT, the overall uptake of BMV was increased and provide

167 hanced from both polymers in the presence of MCT.

168 D44, and emmprin contribute to regulation of MCT localization and function in the plasma membrane of

169 iated mRNAs, we showed that up-regulation of MCT-1 was able to modulate the translation profiles of B

170 ein kinases is critical for stabilization of MCT-1 protein and for its ability to promote cell prolif

171 d diminished distal pulmonary vasculature of MCT(sl/sl) rat lungs.

172 Importantly, the effects of MCTs could be mimicked by adding Pluronic L81 to LCTs, a

173 Compared with corn oil, MCT supplements had no significant effect on plasma lipo

174 otein) and extracellular CAIV (expressed) on MCT transport activity, were additive.

175 indicating the removing of oxidized films on MCT wafers, which is difficult to achieve using single H

176 observed in electrochemical measurements on MCT wafers.

177 nvestigate the effects of DNA methylation on MCT expression and lactate transport in SMCs in relation

178 5, and 4.74 nm are achieved, respectively on MCT wafers after CMP.

179 Overexpression of a novel oncogene MCT-1 (multiple copies in a T cell malignancy) causes ma

180 vidually (Ligatin) or together (the oncogene MCT-1 and DENR, which are homologous to N-terminal and C

181 nificant sequence homology with the oncogene MCT-1.

182 in terms of protease content (tryptase-only [MCT], tryptase + chymase [MCTC]) and tumour necrosis fac

183 mice after 6-8 weeks of saline (control) or MCT (600 mg/kg) injections.

184 ped for mercury cadmium telluride (HgCdTe or MCT) semiconductors.

185 mRNA are released by eIF1/eIF1A, Ligatin, or MCT-1/DENR.

186 ing a so-called minimal control topology, or MCT).

187 Inhibition of HDACs or MCTs decreases acetate export and lowers pH(i), particul

188 Outward MCT activity is, however, thermodynamically inhibited by

189 he advantage of junctional transmission over MCT in vivo.

190 erapeutic strategies to inhibit or overwhelm MCT.

191 The consensus equation (peak MCT should be>1.2x baseline tryptase+2 mg/L) has been pr

192 rtile range (IQR) time from reaction to peak MCT was 1.34 (0.82-2.51) hours.

193 Finally, the polished MCT wafers are cleaned and dried by deionized water and

194 hondrocyte maturation) than in proliferative MCT cells.

195 to HIIT at 90% to 95% of maximal heart rate, MCT at 60% to 70% of maximal heart rate, or RRE.

196 s index 62.14%) or control animals receiving MCT injection alone (PABP 49.67+/-3.22 mmHg; RV/WH ratio

197 Although VEGF increases RBF and reduces MCT, HGF did not affect either.

198 cells use the glycolytic pathway and require MCTs to efflux lactate that results from glycolysis.

199 stacyclin synthase-expressing ELPCs reversed MCT-induced PAH.

200 Timed serial MCT measurements were mapped against the consensus equat

201 Specifically, MCT metabolites and other hypertensive conditions are kn

202 vel MIR sensing approach utilizes structured MCT chips fabricated via molecular beam epitaxy (MBE) as

203 d nitrogen cooled mercury cadmium telluride (MCT) detector and compare their performance to a commerc

204 eguides made from mercury-cadmium-telluride (MCT)-a material to date exclusively used for mid-infrare

205 as a treadmill-based maximum capacity test (MCT).

206 The methacholine challenge test (MCT) is commonly used to assess airway hyperresponsivene

207 n was also considerably higher for LCT- than MCT-emulsions, which may impact the subsequent absorptio

208 n E after digestion was higher for LCT- than MCT-emulsions, which was attributed to the greater solub

209 Herein we establish that MCT-1 is highly expressed in 85% of human diffuse large

210 Here, we established that MCT-1 protein interacts with the cap complex through its

211 We find that MCT-1 is phosphorylated and up-regulated by extracellula

212 tion-related defects, strongly implying that MCT-1 functions in translation-related processes.

213 ng with Raman micro-spectroscopy showed that MCT was primarily confined to the inclusions within the

214 Such studies suggest that MCT consumption may be useful for weight management.

215 Taken together, our results suggest that MCT-1 may contribute to the pathogenesis and progression

216 The MCT isoforms 1 and 4 are the major isoforms of this tran

217 The MCT-1 oncogene was originally identified from lymphoma c

218 The MCT-1 protein is predicted to have numerous putative pho

219 t analyses demonstrated that patients in the MCT group had significantly greater reductions in the co

220 lyses also demonstrated that patients in the MCT group had significantly greater reductions in the PA

221 ydrophobic films, it was more soluble in the MCT inclusions in hydrophilic films, suggesting its incr

222 ixed-abrasive lapping is used to machine the MCT wafers, and the lapping solution is deionized water.

223 In a breast tumor xenograft model, the MCT-1 oncogene increases the in vivo tumorgenicity of MC

224 into account the reduced sensitivity of the MCT in white and nonatopic asthmatic patients when using

225 Administration of the MCT inhibitor l-lactate increased GHB renal and total cl

226 We investigated the ability of the MCT to differentiate participants with a physician's dia

227 The utility of the MCT to rule out a diagnosis of asthma depends on racial

228 We sought to determine if disruption of the MCT-Basigin interaction may be achieved with a small mol

229 luate the sensitivity and specificity of the MCT.

230 se findings highlight that inhibition of the MCT/BSG complexes alone or in combination with phenformi

231 The synergistic activities of the MCT/CD147 complex could facilitate migration of tumor ce

232 Secondly, the MCT wafers are polished using the developed CMP slurry.

233 The flux of lactate and protons through the MCT plays an important role in muscle energy metabolism

234 psychological training group relative to the MCT group.

235 factors (the first of these is unique to the MCT simulations while the other two seem to be general p

236 directly interfacing the waveguide with the MCT detector element may be envisaged.

237 f enzyme kinetics: metabolic control theory (MCT) and Michaelis-Menten saturation kinetics (SK).

238 Phenformin addition to these MCT-disrupted cells in normoxic and hypoxic conditions i

239 of magnitude upon implementation of thinner MCT waveguides.

240 blood flow (RBF) and mean circulation time (MCT) were evaluated by video fluorescein angiography.

241 door biting (POB) and median catching times (MCT) were compared.

242 The mutable collagenous tissue (MCT) of echinoderms (e.g., sea cucumbers and starfish) i

243 ng the macromolecular competition titration (MCT) method.

244 Administration of AP-Cav to MCT rats significantly reduced the right ventricular sys

245 increases in CD147 expression were linked to MCT expression in MDA-MB-231, a highly metastatic breast

246 ion of a Cav-based cell-permeable peptide to MCT rats prevents the development of pulmonary artery me

247 HIIT was not superior to MCT in changing left ventricular remodeling or aerobic c

248 is superior to moderate continuous training (MCT) in reversing cardiac remodeling and increasing aero

249 Metacognitive training (MCT) is targeted at cognitive biases involved in the pat

250 have developed a novel mucociliary transit (MCT) measurement that uses synchrotron phase contrast X-

251 Mucociliary transport (MCT) is an innate defense mechanism that removes particu

252 d (PCL) hydration and mucociliary transport (MCT) rates, a relationship frequently invoked but never

253 rized by a deficit in mucociliary transport (MCT), a process that traps and propels bacteria out of t

254 nopeptidase CD13 and the lactate transporter MCT-1.

255 ks the neuronal monocarboxylate transporter (MCT) 2 but not the astrocytic MCTs (MCT1 and MCT4).

256 The monocarboxylate transporter (MCT) family member MCT1 can transport lactate into and o

257 inhibition and monocarboxylate transporter (MCT) inhibition were assessed by inhibitor administratio

258 iffusion and by monocarboxylate transporter (MCT) mediated transport.

259 Monocarboxylate transporter (MCT)-1, a member of a family of molecules, transports mo

260 Monocarboxylate transporters (MCT) are important regulators of cellular bioenergetics,

261 Monocarboxylate transporters (MCT) modulate tumor cell metabolism and offer promising

262 inhibitors for monocarboxylate transporters (MCT) or replacing LA with sodium lactate revealed that L

263 is mediated by monocarboxylate transporters (MCT), which are composed of a catalytic unit (MCT) and a

264 s with various monocarboxylate transporters (MCT).

265 onocarboxylate lactate-H(+) co-transporters (MCTs) with AR-C155858.

266 Proton-coupled monocarboxylate transporters (MCTs) are carriers of high-energy metabolites such as la

267 Proton-coupled monocarboxylate transporters (MCTs) mediate the exchange of high energy metabolites li

268 of the cell by monocarboxylate transporters (MCTs), preventing further reductions in pH(i).

269 nd protons via monocarboxylate transporters (MCTs), which exacerbates extracellular acidification and

270 up lactate via monocarboxylate transporters (MCTs), which we identify as MCT1 by confocal immunofluor

271 tate efflux on monocarboxylate transporters (MCTs).

272 ocytes through monocarboxylate transporters (MCTs).

273 rols (LCT) or medium chain triacylglycerols (MCT) as carrier oils.

274 onsumption of medium-chain triacylglycerols (MCTs) leads to greater energy expenditure than does cons

275 ating the lipidic medium-chain triglyceride (MCT) into polymeric film-forming systems (FFS) for topic

276 either saturated medium chain triglyceride (MCT) oil or unsaturated purified linseed oil (LSO), were

277 Orange oil, medium-chain triglyceride (MCT) oil, and WPI were used to make stable nanoemulsions

278 Medium-chain triglyceride (MCT) supplements are used by clinicians to treat patient

279 oil composition (medium-chain triglyceride (MCT) to long-chain triglyceride (LCT) ratio) and total c

280 following order: medium chain triglycerides (MCT) > corn oil approximately fish oil > orange oil > mi

281 lycerides (LCT), medium chain triglycerides (MCT) or orange oil as carrier oils.

282 l (SO)], MS [50% medium-chain triglycerides (MCTs) and 50% SO], MSF (50% MCTs, 40% SO, and 10% fish o

283 oral gavage with medium-chain triglycerides (MCTs) plus egg white (EW) and was characterized by incre

284 ted that dietary medium-chain triglycerides (MCTs), which bypass mesenteric lymph and directly enter

285 or assessing serum total mast cell tryptase (MCT) in anaphylaxis.

286 high in melanoma and many other tumor types, MCT inhibitors may have broad application in cancer trea

287 However, the mechanism underlying MCT-1 regulation is largely unknown.

288 CT), which are composed of a catalytic unit (MCT) and an accessory subunit (CD147), comprising the fu

289 However, it remains uncertain whether MCT abnormalities contribute to the genesis of disease o

290 = 0.071) and trunk fat mass (P = 0.10) with MCT consumption than with olive oil.

291 exposed to hypoxia and rats challenged with MCT in response to Imatinib treatment.

292 ng a signaling molecule that correlated with MCT performance in the AE conditions, but also highly co

293 copy imaging and nanoindentation of FFS with MCT revealed two-phase structured films with softer incl

294 or TSLP mAbs before initial oral gavage with MCT/EW to suppress FA development; treatment with the sa

295 The chimeric animals were injected with MCT to produce pulmonary hypertension.

296 abdominal adipose tissue were all lower with MCT consumption than with olive oil consumption (all una

297 A single gavage of peanut protein with MCT, as well as prolonged feeding in MCT-based diets, ca

298 The LV of rats with MCT-induced RVF exhibited electrophysiologic remodeling:

299 ndicate that short-term supplementation with MCT has a neutral effect on TRL apo B-48 and VLDL apo B-

300 ic hydroxypropyl cellulose, with and without MCT.