Effects Of Ethanolamine Research Articles

Effect of ethanolamine as a steel corrosion inhibitor in realkalization of carbonated concrete

ABSTRACT This paper assessed the electromigration behavior of ethanolamine and its efficiency as a corrosion inhibitor of rebar during the realkalization. Cylindrical concrete specimen (diameter 45 mm, height 20 mm) with steel rebar (6 mm in diameter, 35 mm in length) were artificially carbonated and corroded in an accelerated manner with impressed anodic current. The specimens were realkalized in the electrolyte solution containing ethanolamine, while the steel rebars were connected to the cathodic current (200 mA·h, 1 A/m2). After 25 days of monitoring the repair process, experimental data revealed notable changes in electrochemical parameters. The corrosion potential increased from −627 mV to −236 mV, signifying a reduction in corrosion activity. The cathodic exchange current density decreased from 4.9 μA/cm2 to 2.3 μA/cm2, showing a decrease in the corrosion rate. Also, the pH value of the solution dropped to a comparatively lower level, the ethanolamine and potassium ion concentrations decreased from 22 to 30.54 g/L to 3.22 and 10.23 g/L, respectively. Moreover, nitrogen detection on the steel surface and varied levels of ethanolamine concentration at different depths in the concrete were also measured, both indicating a clear migration of inhibitor to the steel surface to form a passive film.

Effect of ethanolamine utilization on the pathogenicity and metabolic profile of enterotoxigenic Escherichia coli.

Bacterial pathogenicity is greatly affected by nutrient recognition and utilization in the host microenvironment. The characterization of enteral nutrients that promote intestinal pathogen virulence is helpful for developing new adjuvant therapies and inhibiting host damage. Ethanolamine (EA), as a major component of intestinal epithelial cells and bacterial membranes, is abundant in the intestine. Here, we provide the first demonstration that the critical human and porcine pathogen enterotoxigenic Escherichia coli (ETEC) can utilize EA as a nitrogen source, which affects its virulence phenotype. We found that compared with that in M9 medium (containing NH4Cl), EA inhibited ETEC growth to a certain extent; however, the relative expression levels of virulence-related genes, such as ltA (3.0-fold), fimH (2.9-fold), CfaD (2.6-fold), gspD (3.6-fold), and qesE (1.3-fold), increased significantly with 15mM EA as a nitrogen source (P < 0.05), and the adhesion efficiency of ETEC to Caco-2 cells increased approximately 4.2-fold. In Caco-2 cells, the relative cell viability decreased from 74.8 to 63.4%, and the transepithelial electrical resistance (TEER) cells decreased to 74.8% with intestinal EA (4mM). In addition, the relative expression levels of proinflammatory factors, such as TNF-α (3.2-fold), INF-γ (2.9-fold), and IL-1β (1.98-fold), in ETEC-infected Caco-2 cells were significantly upregulated (P < 0.05) under EA exposure; however, the above virulence changes were not found in ΔeutR and ΔeutB ETEC. A gas chromatography-mass spectrometry (GC-MS)-based untargeted metabolomics approach was then employed to reveal EA-induced metabolic reprogramming related to ETEC virulence. The data showed that most metabolites related to carbohydrate, aspartate and glutamate metabolism, shikimic acid metabolism, and serine metabolism in ETEC exhibited a decreasing trend with increases in the EA concentration from 0 to 15mM, but the branched-chain amino acid (BCAA) levels in ETEC increased in a dose-dependent manner under EA exposure. Our data suggest that the intestinal EA concentration can significantly affect the virulence phenotype, metabolic profile, and pathogenicity of ETEC. KEY POINTS: • ETEC growth and virulence gene expression could be regulated by ethanolamine. • The intestinal concentration of EA promoted the damaging effect of ETEC on the host epithelial barrier. • The promoting effect of EA on ETEC toxicity may be related to BCAA metabolism.

Effect of Ethanolamine and HCl on structural and optical properties of Nickel oxide thin films

In the present work, Nickel Oxide thin films were prepared by spin coating technique. The effects of Ethanolamine and HCl on structural and optical properties of NiO thin films are studied. The structural properties of NiO thin films were examined by X-ray Diffraction (XRD). The amorphous nature of NiO thin films were observed from XRD pattern. FESEM studies of the surface morphology of NiO thin films exhibits smooth and uniform surface with average particle size of 200 nm for Ethanolamine doping sample and 300 nm for HCl doping sample. The functional groups and surface roughness of NiO thin films were investigated by FTIR and 3 D Laser Profilometry. The surface roughness of the prepared samples increases with increasing thickness from 4.49 μm to 6.81 μm. The optical characteristics of the samples were determined by UV Visible Spectrophotometer. This results shows that the prepared NiO thin films exhibits high optical transparency.

Ethanolamine: A Potential Promoiety with Additional Effects on the Brain.

Ethanolamine is a bioactive molecule found in several cells, including those in the central nervous system (CNS). In the brain, ethanolamine and ethanolamine-related molecules have emerged as prodrug moieties that can promote drug movement across the blood-brain barrier. This improvement in the ability to target drugs to the brain may also mean that in the process, ethanolamine concentrations in the brain are increased enough for ethanolamine to exert its own neurological actions. Ethanolamine and its associated products have various positive functions ranging from cell signaling to molecular storage, and alterations in their levels have been linked to neurodegenerative conditions such as Alzheimer's disease. This mini-review focuses on the effects of ethanolamine on the CNS and highlights the possible implications of these effects for drug design.

Effect of ethanolamine and nano-TiO2 on the properties of ferrocement composites under different exposure environments

Effect of ethanolamine and nano-TiO2 on the properties of ferrocement composites under different exposure environments

Effect of Ethanolamine on Corrosion Behavior of WB36CN1 Steel in Simulated Secondary Circuit of Pressurized Water Reactor

Effect of Ethanolamine on Corrosion Behavior of WB36CN1 Steel in Simulated Secondary Circuit of Pressurized Water Reactor

Effect of ethanolamine passivation of ZnO nanoparticles in quantum dot light emitting diode structure

The aging of ZnO nanoparticles in quantum dot light-emitting diode (QD-LED) structures was studied. Coarsening of as-synthesized ZnO nanoparticles is observed in both solution and thin film structures, which potentially deteriorates the performance of QD-LED devices over time. First, the temperature effect on ZnO coarsening was investigated, and it was revealed that aging of ZnO nanoparticles is faster at higher temperature due to a diffusion-controlled mechanism of nanoparticle coarsening. To observe aggregation of ZnO in the film state, the electron transporting part (ZnO/Al) of the QD-LED structure was prepared. The current density of a ZnO film and an electron-only device (QD/ZnO between two electrodes) was also measured. Resistance of the film increased as a function of aging time, which corresponded with observations of the ZnO film by optical microscopy. Aggregation of ZnO nanoparticles was directly measured by the root-mean-square value using atomic force microscopy. Ethanolamine (EA) stabilizer was added to the ZnO solution to disperse the ZnO nanoparticles without aggregation. The effect of EA on the surface passivation of the ZnO found to suppress pinhole formation, as revealed by scanning electron microscopy observations. Finally, the device lifetime was measured for QD-LEDs with EA-stabilized ZnO to understand the effect of ZnO aging on long-term QD-LED device operation.

Effect of Ethanolamine, Ammonia, Acetic Acid, and Formic Acid on Two-Phase Flow Accelerated Corrosion in Steam–Water Cycles

Effects of ethanolamine, ammonia, and acetic and formic acid on two-phase flow-accelerated corrosion were investigated in an experimental loop simulating the conditions found in a water-steam cycle. Results indicate that the effects of acetic acid and ethanolamine on the corrosion rate neutralize each other. The effect of acetic acid on the corrosion rate was most pronounced at the highest tested steam quality. A model simulation for liquid film pH at 90% steam quality suggests that at very high steam qualities the protection ethanolamine provides increases, while the protection provided by ammonia goes down. A linear relation between calculated liquid film pH and the measured corrosion rate was found for 24% steam quality within a pH range from 5.6 to 6.3. Formic acid was thermally unstable at the tested temperatures and had no effect on the corrosion rate.

Influence of Ethanolamine on Corrosion of Alloy 690 in Simulated Secondary Water

Effect of ethanolamine (ETA) on Alloy 690 in simulated pressurized water reactor (PWR) secondary cooling water was studied by electrochemical impedance spectroscopy (EIS), potentiodynamic polarization, atomic force microscopy (AFM), Fourier transform infrared spectroscopy-attenuated total reflectance (FTIR-ATR), X-ray photoelectron spectrometer (XPS) and time of flight secondary ion mass spectrometry (ToF-SIMS). The results show that moderate addition of ETA can enhance the corrosion resistance of Alloy 690 in high-temperature pressurized water and the optimum additive value is 2 mg/L. The addition of ETA contributes to the formation of oxide rather than hydroxide in the film on the surface of Alloy 690. The corrosion resistance of Alloy 690 at 320 °C with the addition of ETA is better than that at 280 °C.

Low temperature aqueous precipitation of needle-like nanophase hydroxyapatite

The use of tissue engineered biodegradable porous scaffolds has become an important focus of the biomedical research field. The precursor materials used to form these structures play a vital role in their overall performance thus making the study and synthesis of these selected materials imperative. The authors present a comparison and characterisation of hydroxyapatite (HA), a popular calcium phosphate (CaP) biomaterial, synthesised by an aqueous precipitation (AP) method. The influence of various reaction conditions on the phase, crystallinity, particle size as well as morphology, molecular structure, potential in-vivo bioactivity and cell viability were assessed by XRD, SEM and TEM, FTIR, a simulated body fluid (SBF) test and a live/dead assay using MC3T3 osteoblast precursor cells, respectively. Naturally carbonated nanoparticles of HA with typically needle-like morphology were synthesised by the reported AP method. Initial pH was found to influence the crystallisation process and determine the CaP phase formed as well as the resultant particle and crystallite sizes. A marked change in particle morphology was also observed above pH 9. The use of toluene as a replacement solvent for water up to 60% was found to reduce the crystallinity of as-synthesised HA. This has marked influence on the effect of ethanolamine (5 wt%), which was found to improve HA crystallinity. SEM and EDS were used to confirm the growth of carbonated apatite on the surface of HA pellets immersed in SBF for up to 28 days. Cell culture results revealed viable cells on all samples where pH was controlled and maintained at 10-11 during precipitation, including those that used ethanolamine and toluene in preparation. When the initial alkali pH was not maintained non-viable cells were observed on HA substrates.

Ethanolamine is a novel STAT-3 dependent cardioprotective agent

Ethanolamine is a biogenic amine found naturally in the body as part of membrane lipids and as a metabolite of the cardioprotective substances, sphingosine-1-phosphate (S1P) and anandamide. In the brain, ethanolamine, formed from the breakdown of anandamide protects against ischaemic apoptosis. However, the effects of ethanolamine in the heart are unknown. Signal transducer and activator of transcription 3 (STAT-3) is a critical prosurvival factor in ischaemia/reperfusion (I/R) injury. Therefore, we investigated whether ethanolamine protects the heart via activation of STAT-3. Isolated hearts from wildtype or cardiomyocyte specific STAT-3 knockout (K/O) mice were pre-treated with ethanolamine (Etn) (0.3 mmol/L) before I/R insult. In vivo rat hearts were subjected to 30 min ischaemia/2 h reperfusion in the presence or absence of 5 mg/kg S1P and/or the FAAH inhibitor, URB597. Infarct size was measured at the end of each protocol by triphenyltetrazolium chloride staining. Pre-treatment with ethanolamine decreased infarct size in isolated mouse or rat hearts subjected to I/R but this infarct sparing effect was lost in cardiomyocyte specific STAT-3 deficient mice. Pre-treatment with ethanolamine increased nuclear phosphorylated STAT-3 [control 0.75 ± 0.08 vs. Etn 1.50 ± 0.09 arbitrary units; P < 0.05]. Our findings suggest a novel cardioprotective role for ethanolamine against I/R injury via activation of STAT-3.

Actions of ethanolamine on cultured sensory neurones from neonatal rats

Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca 2+ imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1 μM) increased the mean Ca 2+ transient produced by 1 mM caffeine and modulated Ca 2+ transients evoked by 60 mM KCl. Thapsigargicin (500 nM) inhibited the ethanolamine-evoked enhancement of Ca 2+ transients evoked by depolarisation. Voltage-activated K + currents were evoked from a holding potential of −70 mV by voltage step commands to 0 mV. Acute application of 1 μM ethanolamine produced irreversible current modulation. However, application of 100 nM ethanolamine reversibly increased or decreased K + currents. These effects of ethanolamine on voltage-activated K + currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500 nM) had no action on the mean K + current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K + channels and a component of intracellular Ca 2+ signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.

Nanosize Mn 3O 4 (Hausmannite) by microwave irradiation method

The present investigation reports, the novel synthesis of nanosize Mn 3O 4 powder with nanorods using microwaves and its physicochemical characterization. The nanosize Mn 3O 4 powder has been prepared using manganese nitrate as a precursor and effect of ethanolamine and ethylenediamine on particle morphology has been studied. The microwave irradiation has been carried out in the range 50–500 W and it was observed that formation of Mn 3O 4 takes place at 50 W. TEM analysis demonstrated nanosize Mn 3O 4 powder and nanorods with an average diameter of about 10 nm. The structural study by XRD indicates that these nano-powders have pure tetragonal phase. The phase pure samples were characterized using X-Ray Photoelectron Spectroscopy (XPS) for both Mn 2p and Mn 3s levels. The values of binding energies are consistent with the relative values reported in the literature. The metallic impurity levels have been characterized using Inductively Coupled Plasma-Optical Emission Spectrophotometer (ICP-OES).

Effect of ethanolamine on liver regeneration after 90% hepatectomy in rats

SURGICAL PROCEDURES, such as extended liver resection or living-related liver transplantation may be performed because normal liver has vigorous regenerative potential. However, reduced hepatic volume can produce postoperative hepatic insufficiency, which is a serious problem. After extensive liver resection for hepatic tumor or in living-related liver donors maximum volume of liver resection or thus the minimum volume of donor liver are limited. When the volume exceeds these limits, surgical treatment is not indicated. However, a new treatment that promotes postoperative liver regeneration would extend these limits. Two approaches have been attempted to promote liver regeneration. One approach prepares the host environment for liver regeneration by plasma exchange. In recent years, favorable results also have been reported using a bioartificial liver as a bridge. The other approach is promotion of liver regeneration using hepatocyte growth factor (HGF) or ethanolamine (EA). EA is a nutrient factor derived from the small intestine. In this study, we investigated the enhancing effect of EA using a 90% partial hepatectomy (PHX) rat model.

Phosphorylation of ethanolamine, methylethanolamine, and dimethylethanolamine by overexpressed ethanolamine kinase in NIH 3T3 cells decreases the co-mitogenic effects of ethanolamines and promotes cell survival.

Ethanolamine (Etn), as well as its N-methyl (MeEtn) and N,N-dimethyl (Me2Etn) analogues, were recently shown to potentiate the stimulatory effect of insulin on DNA synthesis in serum-starved NIH 3T3 fibroblasts. In the present work we assessed the impact of the co-mitogenic effects of Etn and its methyl analogues on cell proliferation and cell survival, and examined whether the cell growth regulatory effects of these ethanolamines involve an Etn-kinase-mediated phosphorylation step. For this purpose, NIH 3T3 sublines highly overexpressing Drosophila Etn kinase and an appropriate vector control line were utilized and the effects of Etn, MeEtn, Me2Etn, methylamine (MeNH2), and dimethylamine (Me2NH) were studied. 31P-NMR analysis of the water-soluble cell metabolites revealed that both MeEtn and Me2Etn, but not choline, are excellent substrates for the expressed Etn kinase. The methylated ethanolamines (MeEtn and Me2Etn) and methylamines (MeNH2, Me2NH) were used as Etn models that can or cannot be phosphorylated, respectively. In serum-starved vector control cells, both MeNH2 (1 mM) and Me2NH (1 mM) were more effective than Etn in enhancing insulin-induced DNA synthesis, and both were almost as effective as MeEtn and Me2Etn. However, in the Etn kinase overexpressor cells the potentiating effects of Etn, MeEtn and Me2Etn, but not those of MeNH2 and Me2NH, were significantly reduced. Moreover, in the overexpressor cells, lower concentrations of Etn (50-200 microM) inhibited the combined mitogenic effects of Me2NH (1 mM) and insulin. These data are consistent with a mechanism in which the phosphorylated and non-phosphorylated ethanolamines are negative and positive regulators of insulin-induced mitogenesis, respectively. After incubating the cells for 13 days in serum-free medium in 96-well microplates, there was a steady decrease in cell numbers in both cell lines. However, between 6-13 days, 0.1-1 mM MeEtn and, particularly, Me2Etn provided significant protection against cell death in the Etn kinase overexpressor cells. In vector control cells, only Me2Etn in combination with insulin had similar effects on cell survival. The data suggest that phosphorylated ethanolamines may function as promoters of cell survival.

The Clinical and Histological Effects of Ethanolamine in Varicose Veins

Objective: To study the histological changes in varicosities after injection of 5% ethanolamine. Design: A prospective study in nine groups of six patients awaiting bilateral varicose vein surgery. Patients: Each patient had a below-knee incompetent perforating vein injected with either 0.5, 1.0 or 2.0 ml 5% ethanolamine. The contralateral varicosity received a similar volume of normal saline. Intervention: The patients wore elasticated stockings until admitted for operation at 2, 4 or 8 weeks after the injections. The injected varicosity was then dissected out. Main outcome measures: Each vein was reported on by a histologist who did not know which had received ethanolamine or saline. The histologist graded each vein according to the severity of change from 0 (no effect) to 5 (total obliteration of vein). Results: Ethanolamine at 0.5, 1.0 and 2.0 ml caused extensive histological damage to the varicosity. After 8 weeks most varicosities had been destroyed. Conclusion: Ethanolamine, unlike sodium tetradecyl sulphate, causes complete destruction of a varicosity. A dose of 0.5 ml is just as effective as 2.0 ml.

The effect of ethanolamine on acute carbon tetrachloride intoxication.

The effects of ethanolamine on injured liver were investigated by oral administration of ethanolamine to male ddY mice 24 h after carbon tetrachloride (CCl4) injection. The serum aminotransferase activities in mice with liver injury were reduced by ethanolamine treatment (10-30 mg/kg body weight). Drastically increased regenerative reaction of ethanolamine treated-CCl4 injured liver was also observed through an increase in 5-bromo-2'-deoxyuridine uptake. ATP concentration in liver tissue was recovered by administration of ethanolamine. These results suggest that oral administration of ethanolamine accelerates recovery from CCl4-induced liver injury.

Effects of ethanolamine (Etn) administration on Etn and choline (Ch) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: an in vivo study.

The sources and fates of brain ethanolamine (Etn) are poorly known and the effects of its administration have not been investigated, even though cortical levels are known to be reduced in certain neurodegenerative diseases. We studied the effect of different Etn doses (10(-3), 5 x 10(-3) and 10(-2) mol/kg, i. p.) on its and choline's (Ch) levels in arterial plasma and brain extracellular fluid (ECF) of awake rats. We also studied its effects on brain levels of Etn, Ch, and their respective major phospholipids. Etn administration caused dose dependent increases in Etn levels within both plasma and brain ECF. For the 10(-2) mol/kg dose, Etn levels were significantly (p<0.01) greater than pre-injection values in both the plasma and ECF. Whole brain Etn and phosphatidylethanolamine were also significantly (p<0.05) increased by 10(-2) mol/kg Etn. Exogenous Etn significantly (p<0.05) increased Ch levels in plasma and whole brain; Etn also increased brain ECF Ch levels. Our data show for the first time that circulating Etn can act as a source of brain Ch. Metabolic pathways that might mediate the increases in Etn and Ch are discussed, as are possible mechanisms of the decreases in brain Eth seen in Alzheimer's disease.

Effects of ethanolamine (ETN) administration on ETN and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

The sources and fates of brain ethanolamine (Etn) are poorly known and the effects of its administration have not been investigated, even though cortical levels are known to be reduced in certain neurodegenerative diseases. We studied the effect of different Etn doses (10−3, 5 × 10−3 and 10−2 mol/kg, i. p.) on its and choline's (Ch) levels in arterial plasma and brain extracellular fluid (ECF) of awake rats. We also studied its effects on brain levels of Etn, Ch, and their respective major phospholipids. Etn administration caused dose dependent increases in Etn levels within both plasma and brain ECF. For the 10−2 mol/kg dose, Etn levels were significantly (p<0.01) greater than pre-injection values in both the plasma and ECF. Whole brain Etn and phosphatidylethanolamine were also significantly (p<0.05) increased by 10−2 mol/kg Etn. Exogenous Etn significantly (p<0.05) increased Ch levels in plasma and whole brain; Etn also increased brain ECF Ch levels. Our data show for the first time that circulating Etn can act as a source of brain Ch. Metabolic pathways that might mediate the increases in Etn and Ch are discussed, as are possible mechanisms of the decreases in brain Etn seen in Alzheimer's disease.

The Synergetic Effect of Ethanolamine and Benzotriazole on the Corrosion Inhibition of Copper

The Synergetic Effect of Ethanolamine and Benzotriazole on the Corrosion Inhibition of Copper