EtOH Concentrations Research Articles

On the phase behavior of the quaternary system acrylic acid-water-ethanol-CO2 by in situ infrared spectrometry

The phase equilibrium of acrylic acid (AA)/carbon dioxide (CO2) as well as mixtures containing water, AA, CO2 and/or ethanol (EtOH) has been investigated. An in-situ infrared analysis method combining FTIR and ATR-IR spectrometry techniques has been used to obtain concentrations of each component in both phases, i.e. CO2-rich and water-rich ones, as a function of pressure and temperature. Measurements have been performed at 65 and 75°C for pressures ranging between 0.1 and 20MPa. The solubilities of AA, water and EtOH in the CO2-rich phase and the concentrations of AA, EtOH and CO2 in the water-rich phase have been obtained. From these measurements, a complete phase diagram of the binary AA-CO2 system as well as the partition coefficient of each component in the quaternary system have been established. It has been demonstrated that AA is in equilibrium between the water- and the CO2-rich phases and that EtOH limits this transfer. Nevertheless, aqueous droplets of AA in CO2 at high pressure can be used as monomer reservoirs releasing the monomer in the CO2-rich phase.

Effect of Intravenous Ethanol on Capsaicin-Induced Hyperalgesia in Human Subjects.

The objective of this study was to assess ethanol's (EtOH's) effects on capsaicin-induced hyperalgesia in healthy participants. Specifically, we investigated the change in area of capsaicin-induced hyperalgesia following 3 interventions: intravenous EtOH at 2 targeted breath alcohol concentrations (BrAC), or placebo. Eighteen participants participated in 3 test days in a randomized order. Each test day, participants received an intradermal capsaicin injection on the volar surface of the forearm, followed by either infusion of high concentration EtOH (targeted BrAC=0.100g/dl), low concentration EtOH (targeted BrAC=0.040g/dl), or placebo. The area of hyperalgesia was determined by von Frey technique at 2 time points, prior to EtOH infusion, and again when target BrAC was reached. The primary outcome was the percent change in the area of capsaicin-induced hyperalgesia. Additional outcome measures included the visual analogue scale of mood states (VAS), which was administered at each time point. There was a marked 30% reduction in the area of capsaicin-induced hyperalgesia with infusion of a high concentration of EtOH (p<0.05). Low concentration EtOH produced a 10% reduction in hyperalgesia area, although this finding did not reach significance. Further, participants reported significant feelings of euphoria and drowsiness at high concentrations of EtOH (p<0.05), as measured by the VAS. In a human model examining pain phenomena related to central sensitization, this study is the first to demonstrate that capsaicin-induced hyperalgesia is markedly attenuated by EtOH. The capsaicin experimental pain paradigm employed provides a novel approach to evaluate EtOH's effects on pain processing. The antihyperalgesic effects of EtOH observed have important clinical implications for the converging fields of substance abuse and pain medicine and may inform why patients with chronic pain often report alcohol use as a form of self-medication.

Solvent stimulated actuation of polyurethane-based shape memory polymer foams using dimethyl sulfoxide and ethanol

Solvent exposure has been investigated to trigger actuation of shape memory polymers (SMPs) as an alternative to direct heating. This study aimed to investigate the feasibility of using dimethyl sulfoxide (DMSO) and ethanol (EtOH) to stimulate polyurethane-based SMP foam actuation and the required solvent concentrations in water for rapid actuation of hydrophobic SMP foams. SMP foams exhibited decreased Tg when submerged in DMSO and EtOH when compared to water submersion. Kinetic DMA experiments showed minimal or no relaxation for all SMP foams in water within 30 min, while SMP foams submerged in EtOH exhibited rapid relaxation within 1 min of submersion. SMP foams expanded rapidly in high concentrations of DMSO and EtOH solutions, where complete recovery over 30 min was observed in DMSO concentrations greater than 90% and in EtOH concentrations greater than 20%. This study demonstrates that both DMSO and EtOH are effective at triggering volume recovery of polyurethane-based SMP foams, including in aqueous environments, and provides promise for use of this actuation technique in various applications.

Ethanolic Extracts of Copaifera Multijuga Inhibits the Subcutaneous Growth of Ehrlich Carcionoma in Swiss Mice

Oil-resin of Copaifera multijuga Hayne is popularly used due to its anti-inflammatory properties. In this study, we evaluate the effects of the bark ethanolic extract on Ehrlich tumor cells. For extract preparation, bark was removed from stem and chopped into smaller pieces. Most were dried and grounded. The first extract was made with hexane, followed by ethyl acetate. Absolute ethanol was added to the residue and extract was filtered and concentrated (EtOH). In vitro cytotoxic activity of the EtOH was analyzed on both spleen and tumor cells. For evaluation of in vivo activity, Ehrlich carcinoma bearing Swiss mice were daily treated with different concentration of EtOH during 30 days. Evaluation of in vitro cell viability showed that 1mg/ml extract is cytotoxic to spleen and tumor cells. Evaluation of in vivo tumor development showed that treatment with 200mg/kg of EtOH was able to reduce in 45.28% the tumor growth. Treatment for 7 days increased IL-12p70, IFN-γ and TNF-α production and for 14 days reduced the lymphoproliferative activity in both tumor bearing and mice healthy. Our results show that the ethanolic extract of copaiba bark affect Ehrlich tumor cells, reducing their cell viability in vitro as well as their development in vivo.

Clustering mechanism of ethanol-water mixtures investigated with photothermal microfluidic cantilever deflection spectroscopy.

The infrared-active (IR) vibrational mode of ethanol (EtOH) associated with the asymmetrical stretching of the C-C-O bond in pico-liter volumes of EtOH-water binary mixtures is calorimetrically measured using photothermal microfluidic cantilever deflection spectroscopy (PMCDS). IR absorption by the confined liquid results in wavelength dependent cantilever deflections, thus providing a complementary response to IR absorption revealing a complex dipole moment dependence on mixture concentration. Solvent-induced blue shifts of the C-C-O asymmetric vibrational stretch for both anti and gauche conformers of EtOH were precisely monitored for EtOH concentrations ranging from 20–100% w/w. Variations in IR absorption peak maxima show an inverse dependence on induced EtOH dipole moment (μ) and is attributed to the complex clustering mechanism of EtOH-water mixtures.

Transgenerational Transmission of the Effect of Gestational Ethanol Exposure on Ethanol Use-Related Behavior.

Prenatal alcohol exposure (PAE) enhances the risk for alcoholism by increasing the propensity to consume alcohol and altering neurophysiological response to alcohol challenge. Trans-generationally transmittable genetic alterations have been implicated in these behavioral changes. To date, transgenerational transmission of PAE-induced behavioral responses to alcohol has never been experimentally investigated. Therefore, we explored the transgenerational transmission of PAE-induced behavioral effects across 3 generations. Pregnant Sprague Dawley dams received 1g/kg ethanol (EtOH) or water daily on gestational days 17 through 20 via gavage, or remained untreated in their home cages. To produce second filial (F2) or F3 generations, similarly treated adult F1 or F2 offspring were mated and left undisturbed through gestation. On postnatal day (PND) 14, male and female F1, F2, and F3 offspring were tested for consumption of 5% (w/v) EtOH (in water), or water. Using the loss of righting reflex (LORR) paradigm on PND 42, F1 and F2 adolescent male offspring were tested for sensitivity to acute EtOH-induced sedation-hypnosis at 3.5 or 4.5g/kg dose. F3 male adolescents were similarly tested at 3.5g/kg dose. Blood EtOH concentration (BEC) was measured at waking. EtOH exposure increased EtOH consumption compared to both water and untreated control groups in all generations. EtOH-treated group F1 and F2 adolescents displayed attenuated LORR duration compared to the water group. No attenuated LORR was observed in the F3 generation. BEC at waking corroborated with the significant LORR duration differences while also revealing differences between untreated control and water groups in F1 and F2 generations. Our results provide novel behavioral evidence attesting that late gestational moderate EtOH exposure increases EtOH intake across 3 generations and may alter sensitivity to EtOH-induced sedation-hypnosis across 2 generations.

Nest building is a novel method for indexing severity of alcohol withdrawal in mice

Withdrawal after chronic ethanol (EtOH) affects body temperature, goal-directed behavior and motor function in mice and increases general central nervous system excitability. Nest-building tests have been used to assay these states but to this point have not been employed as measures of EtOH withdrawal severity. We first refined nest-scoring methods using a genetically heterogeneous stock of mice (HS/Npt). Mice were then made physically dependent following three days of chronic EtOH vapor inhalation to produce average blood EtOH concentrations (BECs) of 1.89mg/mL. EtOH withdrawal affected the progression of nest building over time when mice were tested 2–4 days after removal from three days of chronic exposure to EtOH. In a separate group of mice, chronic EtOH vapor inhalation (BECs 1.84mg/mL) suppressed nest building over days 1–2 but not days 2–3 of withdrawal. In a following experiment, EtOH withdrawal dose-dependently slowed recovery of nest building for up to 32h. Finally, we determined that long-lasting nest-building deficits extend to mice undergoing withdrawal from a high dose (4g/kg) of acute EtOH. Sex differences for nest building were absent following EtOH exposure. In mice naïve to EtOH treatments, male mice had lower pre-test body temperatures and increased nest scores across a two-day testing period compared to females. These results suggest that nest building can be used to assess chronic and acute EtOH withdrawal severity in mice.

Constants and thermodynamics of the acid-base equilibria of triglycine in water–ethanol solutions containing sodium perchlorate at 298 K

The acid−base equilibrium constants for glycyl-glycyl-glycine (triglycine) in water–ethanol solvents containing 0.0, 0.1, 0.3, and 0.5 mole fractions of ethanol are determined by potentiometric titration at 298.15 K and an ionic strength of 0.1, maintained with sodium perchlorate. It is established that an increase in the ethanol content in the solvent reduces the dissociation constant of the carboxyl group of triglycine (increases pK1) and increases the dissociation constant of the amino group of triglycine (decreases pK2). It is noted that the weakening of the acidic properties of a triglycinium ion upon an increase of the ethanol content in the solvent is due to the attenuation of the solvation shell of the zwitterionic form of triglycine, and to the increased solvation of triglycinium ions. It is concluded that the acid strength of triglycine increases along with a rise in the EtOH content in the solvent, due to the desolvation of the tripeptide zwitterion and the enhanced solvation of protons.

Role of STAT3 Phosphorylation in Ethanol-Mediated Proliferation of Breast Cancer Cells.

PurposeIn this study, we investigated the molecular mechanism involved in ethanol (EtOH)-mediated proliferation of breast cancer cells.MethodsEtOH concentration was optimized by studying its effect on cell proliferation in MCF-7 and MDA MB-231 cells. We used flow cytometry and immunoblot analysis to evaluate the increased proliferation caused by the optimized concentrations of EtOH. The mechanism of EtOH-mediated proliferation was determined using reactive oxygen species (ROS) release assay, reverse transcription polymerase chain reaction, and immunoblot studies. Gene silencing followed by quantitative real-time polymerase chain reaction studies and inhibitor studies indicated the involvement of signal transducer and activator of transcription 3 (STAT3) in EtOH-mediated breast cancer proliferation.ResultsExposure to EtOH caused an increase in cell proliferation and an accumulation of cells in S-phase in MCF-7 (347 µM EtOH) and MDA MB-231 (173 µM EtOH) cells. Additionally, increased release of ROS and the expression of pro-inflammatory cytokines, such as interleukin 6 and tumor necrosis factor α, confirmed that the proliferation was induced by the ROS-linked inflammatory response in breast cancer. The proinflammatory response was followed by phosphorylation of STAT3. The importance of STAT3 activation in EtOH-mediated proliferation was confirmed through the silencing of STAT3, followed by an investigation on the expression of cyclins and matrix metalloproteinases. Finally, studies using specific inhibitors indicated that the EtOH-mediated effect on STAT3 activation could be regulated by phosphoinositide-3-kinase and Janus kinase 2.ConclusionThe study demonstrates the involvement of STAT3 signaling in EtOH-mediated breast cancer proliferation.

Comparison of the response using ICR mice derived from three different sources to ethanol/hydrochloric acid-induced gastric injury.

Animal models for gastric ulcers produced by physical, pharmacological and surgical methods have been widely employed to evaluate therapeutic drugs and investigate the mechanism of action of this disease. ICR mice were selected to produce this model, even though several mice and rats have been widely used in studies of gastric ulcers. To compare the responses of ICR mice obtained from three different sources to gastric ulcer inducers, alterations in gastric injury, histopathological structure, and inflammation were measured in Korl:ICR (Korea NIFDS source), A:ICR (USA source) and B:ICR (Japan source) treated with three concentrations of ethanol (EtOH) (50, 70, and 90%) in 150 mM hydrochloric acid (HCl) solution. Firstly, the stomach lesion index gradually increased as the EtOH concentration increased in three ICR groups. Moreover, a significant increase in the level of mucosal injury, edema and the number of inflammatory cells was similarly detected in the EtOH/HCl treated group compared with the vehicle treated group in three ICR groups. Furthermore, the number of infiltrated mast cells and IL-1β expression were very similar in the ICR group derived from three different sources, although some differences in IL-1β expression were detected. Especially, the level of IL-1β mRNA in 50 and 90EtOH/HCl treated group was higher in Korl:ICR and A:ICR than B:ICR. Overall, the results of this study suggest that Korl:ICR, A:ICR and B:ICR derived from different sources have an overall similar response to gastric ulcer induced by EtOH/HCl administration, although there were some differences in the magnitude of their responses.

Ethanol and Acetaldehyde After Intraperitoneal Administration to Aldh2-Knockout Mice-Reflection in Blood and Brain Levels.

This paper reports, for the first time, on the analysis of ethanol (EtOH) and acetaldehyde (AcH) concentrations in the blood and brains of Aldh2-knockout (Aldh2-KO) and C57B6/6J (WT) mice. Animals were administrated EtOH (1.0, 2.0 or 4.0g/kg) or 4-methylpyrazole (4-MP, 82mg/kg) plus AcH (50, 100 or 200mg/kg) intraperitoneally. During the blood tests, samples from the orbital sinus of the eye were collected. During the brain tests, dialysates were collected every 5min (equal to a 15µl sample) from the striatum using in vivo brain microdialysis. Samples were collected at 5, 10, 15, 20, 25, 30 and 60min intervals post-EtOH and -AcH injection, and then analyzed by head-space GC. In the EtOH groups, high AcH levels were found in the blood and brains of Aldh2-KO mice, while only small traces of AcH were seen in the blood and brains of WT mice. No significant differences in EtOH levels were observed between the WT and the Aldh2-KO mice for either the EtOH dose. EtOH concentrations in the brain were comparable to the EtOH concentrations in the blood, but the AcH concentrations in the brain were four to five times lower compared to the AcH concentrations in the blood. In the AcH groups, high AcH levels were found in both WT and Aldh2-KO mice. Levels reached a sharp peak at 5min and then quickly declined for 60min. Brain AcH concentrations were almost equal to the concentrations found in the blood, where the AcH concentrations were approximately two times higher in the Aldh2-KO mice than in the WT mice, both in the blood and the brain. Our results suggest that systemic EtOH and AcH administration can cause a greater increase in AcH accumulation in the blood and brains of Aldh2-KO mice, where EtOH concentrations in the Aldh2-KO mice were comparable to the EtOH concentrations in the WT mice. Furthermore, detection of EtOH and AcH in the blood and brain was found to be dose-dependent in both genotypes.

Breast cancer 1 (BRCA1)-deficient embryos develop normally but are more susceptible to ethanol-initiated DNA damage and embryopathies

The breast cancer 1 (brca1) gene is associated with breast and ovarian cancers, and heterozygous (+/−) brca1 knockout progeny develop normally, suggesting a negligible developmental impact. However, our results show BRCA1 plays a broader biological role in protecting the embryo from oxidative stress. Sox2-promoted Cre-expressing hemizygous males were mated with floxed brca1 females, and gestational day 8 +/− brca1 conditional knockout embryos with a 28% reduction in protein expression were exposed in culture to the reactive oxygen species (ROS)-initiating drug ethanol (EtOH). Untreated +/− brca1-deficient embryos developed normally, but when exposed to EtOH exhibited increased levels of oxidatively damaged DNA, measured as 8-oxo-2'-deoxyguanosine, γH2AX, which is a marker of DNA double strand breaks that can result from 8-oxo-2'-deoxyguanosine, formation, and embryopathies at EtOH concentrations that did not affect their brca1-normal littermates. These results reveal that even modest BRCA1 deficiencies render the embryo more susceptible to drug-enhanced ROS formation, and corroborate a role for DNA oxidation in the mechanism of EtOH teratogenesis.

Microbiota Protects Mice Against Acute Alcohol-Induced Liver Injury.

Our aim is to investigate the physiological relevance of the intestinal microbiota in alcohol-induced liver injury. Chronic alcohol abuse is associated with intestinal bacterial overgrowth, increased intestinal permeability, and translocation of microbial products from the intestine to the portal circulation and liver. Translocated microbial products contribute to experimental alcoholic liver disease. We subjected germ-free and conventional C57BL/6 mice to a model of acute alcohol exposure that mimics binge drinking. Germ-free mice showed significantly greater liver injury and inflammation after oral gavage of ethanol (EtOH) compared with conventional mice. In parallel, germ-free mice exhibited increased hepatic steatosis and up-regulated expression of genes involved in fatty acid and triglyceride synthesis compared with conventional mice after acute EtOH administration. The absence of microbiota was also associated with increased hepatic expression of EtOH-metabolizing enzymes, which led to faster EtOH elimination from the blood and lower plasma EtOH concentrations. Intestinal levels of EtOH-metabolizing genes showed regional expression differences and were overall higher in germ-free mice relative to conventional mice. Our findings indicate that absence of the intestinal microbiota increases hepatic EtOH metabolism and the susceptibility to binge-like alcohol drinking.

Oral operant ethanol self-administration in the absence of explicit cues, food restriction, water restriction and ethanol fading in C57BL/6J mice.

Mouse models of ethanol (EtOH) self-administration are useful to identify genetic and biological underpinnings of alcohol use disorder. These experiments developed a novel method of oral operant EtOH self-administration in mice without explicitly paired cues, food/water restriction, or EtOH fading. Following magazine and lever training for 0.2 % saccharin (SAC), mice underwent nine weekly overnight sessions with lever pressing maintained by dipper presentation of 0, 3, 10, or 15 % EtOH in SAC or water vehicle. Ad libitum water was available from a bottle. Water vehicle mice ingested most fluid from the water bottle in contrast to SAC vehicle mice, which despite lever pressing demands, drank most of their fluid from the liquid dipper. Although EtOH in SAC vehicle mice showed concentration-dependent increases of g/kg EtOH intake, lever pressing decreased with increasing EtOH concentration and did not exceed that of SAC vehicle alone at any EtOH concentration. Mice reinforced with EtOH in water ingested less EtOH than mice reinforced with EtOH in SAC. EtOH in water mice, however, showed concentration-dependent increases in g/kg EtOH intake and lever presses. Fifteen percent EtOH in water mice showed significantly greater levels of lever pressing than water vehicle mice and a significant escalation of responding across weeks of exposure. Naltrexone pretreatment reduced EtOH self-administration and intake in these mice without altering responding in the vehicle control condition during the first hour of the session. SAC facilitated EtOH intake but prevented observation of EtOH reinforcement. Water vehicle unmasked EtOH's reinforcing effects.

Corticotropin Releasing Factor Binding Protein and CRF2 Receptors in the Ventral Tegmental Area: Modulation of Ethanol Binge Drinking in C57BL/6J Mice.

Most studies with corticotropin releasing factor (CRF) and ethanol (EtOH) consumption have focused on CRF type 1 (CRF1 ) receptors; less is known about other components of the CRF system, such as the CRF type 2 (CRF2 ) receptors and the CRF binding protein (CRFBP). In humans, several nucleotide polymorphisms in the CRFBP gene have been associated with EtOH abuse. The role of the CRFBP within the ventral tegmental area (VTA) and the central nucleus of the amygdala (CeA) was investigated in C57BL/6J mice exposed to an EtOH binge drinking paradigm (drinking in the dark [DID]), or to a dependence-producing drinking protocol (2-bottle choice, intermittent access to alcohol [IAA]) for 4 weeks. Potential interactions between VTA CRFBP and CRF2 receptors on EtOH binge drinking were also assessed. Mice were microinjected with the CRFBP antagonist CRF fragment 6-33 (CRF6-33 ) into the VTA or CeA, or with the CRF2 antagonist astressin-2B (A2B) alone or in combination with CRF6-33 into the VTA, and had access to 20% (w/v) EtOH for 4 hours (DID). Separate cohorts of mice received vehicle and doses of CRF6-33 into the VTA or CeA and had access to EtOH/water for 24 hours (IAA). Blood EtOH concentrations (BECs) were measured, and signs of withdrawal by handling-induced convulsions were determined. Intra-VTA CRF6-33 and A2B reduced EtOH intake dose dependently in mice during DID. Furthermore, a combination of a subeffective dose of CRF6-33 and a lower dose of A2B promoted additive effects in attenuating EtOH binge drinking. Intra-VTA CRF6-33 did not affect EtOH consumption in mice given IAA, and intra-CeA CRF6-33 did not change alcohol consumption in both models of drinking. DID and IAA promoted pharmacologically relevant BECs; however, only mice given IAA exhibited convulsive events during withdrawal. These findings suggest that VTA CRFBP is involved in the initial stages of escalated EtOH drinking by mechanisms that may involve CRF2 receptors.

Anti-diabetic and Anti-oxidative activities of Extracts from Crataegus pinnatifida

This study was performed to investigate the antidiabetic and antioxidant activities of Crataegus pinnatifida which was extracted with water and different concentrations of EtOH (0∼100%). The extraction yield of 70% EtOH (33.16%) was higher than that of 50% EtOH (27.79%), water (21.71%), 30% EtOH (21.88%) and 100% EtOH (19.03%). Total polyphenol contents of 50% EtOH extract from C. pinnatifida were the highest. DPPH and ABTS radical scavenging activities were 80.79±0.83% and 34.92±0.97% in 50% EtOH extract, respectively, which were higher than those of other extracts. The inhibitory activities of 50% ethanol extract from C. pinnatifida against advanced glycation end products (AGEs) formation and α-glucosidase were determined to be 27.09±2.27% and 58.87±0.70%, respectively. The inhibitory activity of water extract from C. pinnatifida against aldose reductase was higher (30.68±1.41%) than those of other extracts. Overall, 50% EtOH extract from C. pinnatifida showed the highest antidiabetic and antioxidant effects. These results suggest that 50% ethanol extracts from C. pinnatifida have potential as a useful ingredient with antidiabetic and antioxidant effects.

Chronic intermittent ethanol exposure in mice leads to an up-regulation of CRH/CRHR1 signaling.

One of the most commonly used approaches to induce ethanol (EtOH) dependence in rodents is EtOH vapor inhalation. This procedure requires the co-administration of pyrazole-an inhibitor of the alcohol dehydrogenase-to obtain stable blood EtOH concentrations (BECs) during the entire induction course. However, pyrazole can produce unwanted side effects. Our goal was to obtain EtOH-dependent mice without pyrazole and to study their behavioral and molecular postdependent phenotype. In particular, we were interested in alterations in the corticotrophin-releasing hormone (CRH) and receptor (CRHR1 and CRHR2) system as a prominent role of CRH in driving the postdependent state via actions in the central extended amygdala (CeA) has been demonstrated in rats but not in postdependent mice. We established an alternative model of chronic intermittent EtOH (CIE) inhalation without the use of pyrazole in C57BL/6N mice. Our CIE exposure protocol involved 8 cycles. One cycle consisted of 8hours with EtOH inhalation and 8hours without EtOH. We then examined withdrawal symptoms. After 2weeks of abstinence, we studied relapse, reinstatement of EtOH-seeking, and stress-induced EtOH self-administration. We also did transcriptional analysis of components of the CRH system during CIE, protracted abstinence, and after stress-induced EtOH self-administration. CIE exposure without pyrazole resulted in reproducible BECs during the induction procedure. Mice showed strong withdrawal scores during 4 to 12hours after the last CIE cycle and enhanced stress-induced EtOH self-administration. This postdependent phenotype during abstinence was accompanied by enhanced Crh and Crhr1 transcripts but no change in Crhr2 transcripts in the CeA. Cue-induced EtOH-seeking behavior and relapse (alcohol deprivation effect) were not affected by the inhalation procedure. We have established a CIE inhalation protocol without pyrazole in mice and showed excessive EtOH self-administration under mild stress and enhanced CRH/CRHR1 signaling in the CeA.

A rapid method for simultaneously determining ethanol and methanol content in wines by full evaporation headspace gas chromatography

This work reports on a full evaporation headspace gas chromatographic (FE HS-GC) method for simultaneously determining the ethanol (EtOH) and methanol (MeOH) content in wines. A small sample (10μL) was placed in a headspace sample vial, and a near-complete mass transfer of ethanol and methanol from the liquid sample to the vapor phase was obtained within three minutes at a temperature of 105°C, which allowed the measurement of the EtOH and MeOH content in the sample by GC. The results showed excellent precision and accuracy, as shown by the reproducibilities of 1.02% and 2.11% for EtOH and MeOH, respectively, and recoveries that ranged from 96.1% to 104% for both alcohols. The method is efficient, accurate and suitable for the determination of EtOH and MeOH in wine production and quality control.

Asymmetric polysulfone gas separation membranes treated by low pressure DC glow discharge plasmas

ABSTRACTAsymmetric polysulfone (PSF) gas separation membranes were prepared at different conditions such as non‐solvent concentration, evaporation time (ET) and coagulation bath temperature (CBT). In addition, effects of low‐pressure DC glow discharge plasma on the characteristics of PSF membranes were investigated. PSF membranes both before and after plasma treatment were characterized by several techniques, including contact angle measurement, scanning electron microscope (SEM), dynamic mechanical thermal analysis (DMTA), and atomic force microscopy (AFM). Furthermore, the performance of membranes was evaluated in terms of permeability of CO2, CH4, O2, and N2 gases. The ideal selectivity of CO2/CH4 and O2/N2 and surface free energy was calculated. Results showed that the EtOH concentration, ET and CBT affect the morphology of PSF membranes. For membranes prepared from a casting solution consisting of PSF 26.0, NMP 28.0, THF 28.0, and EtOH 18.0 wt % and ET for 3 min, the maximum selectivity of untreated membrane is about 69.76 and 12.59 for CO2/CH4 and O2/N2, respectively. After plasma treatment, the ideal selectivity is receded; however, the CO2/CH4 is still higher than 40.41 at pressure of 5 bars. Finally, preparation conditions and DC glow discharge plasmas have significant effects on the characteristics of the PSF membranes and result in an increase of the gas permeation. © 2015 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2015, 132, 42116.

Acetaldehyde, not ethanol, impairs myelin formation and viability in primary mouse oligodendrocytes.

Excessive ethanol (EtOH) drinking is associated with white matter loss in the brain at all stages of life. Myelin-forming oligodendrocytes (OLs) are a major component of white matter, but their involvement in EtOH-mediated white matter loss is unclear. Myelination continues throughout the life with highest rates during fetal development and adolescence. However, little is known about the effects of EtOH and its principal metabolite acetaldehyde (ACD) on OLs at the cellular level. We compared the responses to different concentrations of EtOH or ACD by primary OLs in culture. EtOH did not cause significant cell death at concentrations lower than 120 mM, even after 24 hours. In comparison, ACD was highly lethal at doses above 50 μM. High concentrations of EtOH (120 mM) and ACD (500 μM) for 24 hours did not reduce myelin in mature OLs. Myelin production and OL differentiation were significantly impaired by 7 days exposure to 500 or 50 μM ACD but not 120 mM EtOH. This study shows that OLs are relatively resistant to EtOH, even at a concentration more than 4 times the typical blood EtOH concentrations associated with social drinking (10 to 30 mM). In contrast, OLs are much more sensitive to ACD than EtOH, particularly with long-term exposure. This suggests that part of white matter loss in response to EtOH, especially during high rates of myelin formation, may be due in part to the effects of its principal metabolite ACD.