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Changes or imbalances in plasma amino acid patterns during withdrawal from ethanol were recorded in six randomly selected male chronic alcoholic patients (age range 23-47 years). Duration of drinking ranged from 4-15 years and their average daily amount of ethanol intake was more than 100G. Plasma amino acids (taurine, threonine, serine, glutamate, glutamine, proline, glycine, alanine, cysteine, valine, methionine, isoleucine, leucine, tyrosine, phenylalanine, histidine, tryptophan, ornithine, lysine and arginine) were estimated by autoanalyzer in all patients on admission before starting conventional detoxification therapy for ethanol withdrawal syndrome, and during therapy on day 3 and day 6. On admission, there was a statistically significant rise in the plasma levels of almost all aminoacids, particularly glutamate, glutamine, phenylalanine, proline, glycine, methionine, cysteine, lysine, tyrosine, valine, isoleucine, leucine, serine, threonine, alanine and arginine (in comparison to those of normal controls) in five out of six patients. During the following six days of treatment and total abstinence, the pattern of plasma aminoacid levels did not change significantly despite considerable clinical improvement. Plasma tryptophan levels were undetectable in all patients on admission, day 3 and also on day 6 except in one patient with lesser amount and shorter duration of drinking, the levels just returned to within normal range only on day 6. Plasma levels of histidine and taurine were found to be slightly lower than normal.

Two hundred and fifty‐six consecutive alcoholics admitted for detoxification, but not having delirium tremens, were evaluated for hypertension. Thirty‐three per cent (84) of the alcoholics had a blood pressure ≥ 160/95 mm Hg on or within 72 hr of admission. In 71% (60 of 84) of alcoholics with hypertension, pressure elevation was transitory, whereas 29% (24 of 84) required therapy. After 4 to 5 days of abstinence, alcoholics with transitory hypertension, whose blood pressure was no longer elevated, had a larger increment of pressure (p amp;lt; 0.001) with a cold pressor test than did normotensive alcoholics. Hypertensive alcoholics were older and tended to use greater amounts of alcohol, but their liver enzymes, alcohol levels on admission, and serum magnesium concentrations did not distinguish them from normotensive alcoholics. Basal plasma renin activity and epinephrine were elevated in both hypertensive and normotensive alcoholics, whereas plasma norepinephrine was normal. Although plasma renin activity (4.08 ± 0.9 vs. 2.88 ± 0.4 ng/ml/hr) and epinephrine (138 ± 17 vs. 108 ± 28 pg/ml) were higher in alcoholics with hypertension than in normotensive alcoholics, differences were not significant. However, elevated plasma epinephrine was found in 86% of alcoholics with hypertension, whereas only 44% of normotensive subjects had elevations (x2= 5.49; p = 0.01). Although alcoholics with hypertension demonstrated an exaggerated catecholamine response with the cold pressor test, these changes per se did not explain the elevations in blood pressure. Thus, a transitory, reactive form of hypertension associated with increased catecholamines and vascular hyperresponsiveness is present in alcoholics.

Chronic alcohol consumption induces myocardial damage and a type of non-ischemic cardiomyopathy termed alcoholic cardiomyopathy, where mitochondrial ultrastructural damages and suppressed fusion activity promote cardiomyocyte apoptosis. The aim of the present study is to determine the role of mitochondrial fission proteins and/or other proteins that localise on cardiac mitochondria for apoptosis upon ethanol consumption. In vivo and in vitro chronic alcohol exposure increased mitochondrial Drp1 levels but knockdown of the same did not confer cardioprotection in H9c2 cells. These cells displayed downregulated expression of MFN2 and OPA1 for Bak-mediated cytochrome c release and apoptosis. Dysregulated PTEN/AKT cell survival signal in both ethanol treated and Drp1 knockdown cells augmented oxidative stress by promoting mitochondrial PTEN-L and MFN1 interaction. Inhibiting this interaction with VO-OHpic, a reversible PTEN inhibitor, prevented Bak insertion into the mitochondria and release of cytochrome c to cytoplasm. Thus, our study provides evidence that Drp1-mediated mitochondrial fission is dispensable for ethanol-induced cardiotoxicity and that stress signals induce mitochondrial PTEN-L accumulation for structural and functional dyshomeostasis. Our in vivo results also demonstrates the therapeutic potential of VO-OHpic for habitual alcoholics developing myocardial dysfunction.

Abstract For Solid Oxide Fuel Cells (SOFCs) to become an economically attractive energy conversion technology, suitable materials and structures which enable operation at lower temperatures, while retaining high cell performance, must be developed. Recently, the perovskite-type La 0.6 Ca 0.4 Fe 0.8 Ni 0.2 O 3 oxide has shown potential as an intermediate temperature SOFC cathode. An equivalent circuit describing the cathode polarization resistances was constructed from analyzing impedance spectra recorded at different temperatures in oxygen. A competitive electrode polarization resistance is reported for this oxygen electrode using a Ce 0.8 Gd 0.2 O 1.9 electrolyte, determined by impedance spectroscopy studies of symmetrical cells sintered at 800 °C and 1000 °C. Scanning electron microscopy (SEM) studies of the symmetrical cells revealed the absence of any reaction layer between cathode and electrolyte, and a porous electrode microstructure even when sintered at a temperature of only 800 °C. The performance of this cathode shows favorable oxygen reduction reaction (ORR) properties potentially making it an excellent choice for IT-SOFC application.

Anaphylactic reactions to ethanol are rare with only seven cases reported in the literature. All previous cases have occurred following ingestion of alcoholic beverages or food to which an alcoholic beverage has been added. To date there are no cases in the literature of ethanol-induced anaphylaxis caused by the accumulation of endogenous ethanol in overripe fruit.We report a patient with ethanol-induced anaphylaxis who developed anaphylaxis following ingestion of overripe, but not fresh rock melon (Cucumis melo). The patient is a 24-year-old, previously well woman who experienced five episodes of acute anaphylaxis following ingestion of various alcoholic beverages and, on one occasion, following ingestion of overripe rock melon to which no ethanol was added. Ethanol-induced anaphylaxis was confirmed on blinded challenge; however, challenge with freshly prepared rock melon was negative. The patient declined further challenges.Ingestion of overripe fruits may cause anaphylaxis in patients with ethanol-induced anaphylaxis. These patients should therefore, be advised to avoid ingestion of overripe fruits.

Fatty liver diseases are the most common and major health concern arises from the modern lifestyle and alcohol (ethanol) abuse. The prevalence of non-alcoholic fatty liver diseases (NAFLD) has been observed prominently in obese and diabetic individuals, while alcoholic liver disease is common in alcoholic persons. Fatty liver disease, such as steatohepatitis, leads to fibrosis, cirrhosis and eventually hepatocellular carcinoma. The present study was designed to investigate the effect of 7,8-Dihydroxyflavone (7,8-DHF) against high-fat diet (HFD) and ethanol (EtOH)-induced hepatotoxicity in rats.Male Wistar rats (150-200 g) were fed HFD (58% calories from fat) and EtOH (3-15% in drinking water) for 12 weeks. 7,8-DHF was administered intraperitoneally at the dose of 5 mg/kg/day for the last four weeks. After 12 weeks, biochemical, ELISA, RT-PCR, and histological studies have been carried out.Biochemical analyses revealed the involvement of oxidative stress and inflammation in the liver of HFD and EtOH-fed rats. 7,8-DHF treatment significantly reduced HFD and EtOH-induced oxidative stress as evidenced by the reduction of lipid peroxidation and augmentation of reduced glutathione level. Moreover, IL-1β level was found significantly reduced in 7,8-DHF treated EtOH, HFD and EtOH+HFD groups. The semi-quantitative RT-PCR results indicated down-regulation of Nrf-2 and HO-1 and up-regulation of NF-κB and iNOS mRNA expression level in the liver of HFD and EtOH-fed rats, which was ameliorated by 7,8-DHF treatment.The present study suggested that 7,8-DHF could be an effective pharmacological intervention in combating HFD and EtOH-induced hepatotoxicity.

Human diamine oxidase (hDAO, EC 1.4.3.22) is the key enzyme in the degradation of extracellular histamine. Consumption of alcohol is a known trigger of mast cell degranulation in patients with mast cell activation syndrome. Ethanol may also interfere with enzymatic histamine degradation, but reports on the effects on DAO activity are controversial. There are also conflicting reports whether disulfiram, an FDA-approved agent in the treatment of alcohol dependence, inhibits DAO. We therefore investigated the inhibitory potential of ethanol and disulfiram and their metabolites on recombinant human DAO (rhDAO) in three different assay systems. Relevant concentrations of ethanol, acetaldehyde, and acetate did not inhibit rhDAO activity in an in vitro assay system using horseradish peroxidase (HRP) -mediated luminol oxidation. The aldehyde dehydrogenase (ALDH; EC 1.2.1.3) inhibitors cyanamide and its dimer dicyanamide also had no effect on DAO activity. In one assay system, the irreversible ALDH inhibitor disulfiram and its main metabolite diethyldithiocarbamate seemed to inhibit DAO activity. However, the decreased product formation was not due to a direct block of DAO activity but resulted from inhibition of peroxidase employed in the coupled system. Our in vitro data do not support a direct blocking effect of ethanol, disulfiram, and their metabolites on DAO activity in vivo.

SummaryFollowing ovulation, oocytes undergo a time-dependent deterioration in quality referred to as post-ovulatory ageing. Although various factors influence the post-ovulatory ageing of oocytes, oxidative stress is a key factor involved in deterioration of oocyte quality. Artemisia asiatica Nakai ex Pamp. has been widely used in East Asia as a food ingredient and traditional medicine for the treatment of inflammation, cancer, and microbial infections. Recent studies have shown that A. asiatica exhibits antioxidative effects. In this study, we investigated whether A. asiatica has the potential to attenuate deterioration in oocyte quality during post-ovulatory ageing. Freshly ovulated mouse oocytes were cultured with 0, 50, 100 or 200 μg/ml ethanol extracts of A. asiatica Nakai ex Pamp. After culture for up to 24 h, various ageing-induced oocyte abnormalities, including morphological changes, reactive oxygen species (ROS) accumulation, apoptosis, chromosome and spindle defects, and mitochondrial aggregation were determined. Treatment of oocytes with A. asiatica extracts reduced ageing-induced morphological changes. Moreover, A. asiatica extracts decreased ROS generation and the onset of apoptosis by preventing elevation of the Bax/Bcl-2 expression ratio during post-ovulatory ageing. Furthermore, A. asiatica extracts attenuated the ageing-induced abnormalities including spindle defects, chromosome misalignment and mitochondrial aggregation. Our results demonstrate that A. asiatica can relieve deterioration in oocyte quality and delay the onset of apoptosis during post-ovulatory ageing.

Volatile organic compounds (VOCs) can lead to environmental pollution and threaten human health due to their toxic and carcinogenic nature. The emission of VOCs increases dramatically with the accelerated industrialization and economic growth. Adsorption is identified as one of the most promising recovery technologies owing to its cost-effectiveness, flexible operation, and low energy consumption. In particular, adsorption-based technologies have a high potential to recycle both adsorbents and adsorbates, typically to capture valuable aromatic VOCs from industrial exhaust. Porous materials such as carbon-based materials, zeolite-based materials, and organic polymers and their composites have been extensively developed for VOCs adsorption focusing in adsorption capacity, hydrophobic property, thermal stability and regenerability. Among them, porous carbons as VOCs adsorbents have attracted increasingly attention, because they can be regulated by tuning the pore structure for VOCs accessibility during the adsorption process. Moreover, porous carbons can adsorb target VOCs by controlling the pore structure and surface functional groups. Significantly, the pore size distribution of porous carbons mostly controls the VOCs sorption process. Micropores provide the main adsorption sites, while mesopores enhance the diffusion of VOCs. In this review, the adsorption mechanism of VOCs onto porous carbons was generally concluded. Porous carbons can be designed as a specific structure for adsorption of aromatic VOCs by controlling the pore structure, hydrophobic sites, π-electronic structure, and surface functional groups. Since there are limited review literatures on porous carbons derived from renewable resources for VOCs adsorption, this paper will provide an overview on the synthesis of porous carbons from biomass and other organic wastes for VOCs adsorption or integrated oxidation processes (e.g., photocatalysis, non-thermal plasma catalysis, chemical catalysis) under ambient conditions with the objective of guiding ...