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ABSTRACTA novel design for a high temperature SOFC, based on lamellar electrode-electrolyte segments obtained by solidification of an oxidic eutectic melt on an electrolyte substrate is presented. Such “composite” electrodes contain NiO or MnO - 8Y-ZrO2 lamellae, which after reduction / oxidation yield electrode-electrolyte lamellae with 1–2 μm width and a vertical dimension of> 100 μm, depending upon the amount of eutectic melt solidified on a polycrystalline substrate. The nucleation of the eutectic on a polycrystalline substrate followed by a semi-directional crystallization of the two phases yields a gradient of 3-phase boundaries over the height of such an electrode, with the number of 3-phase boundaries increasing towards the substrate.

Abstract One approach to creating physics-based reduced-order models (ROMs) of battery-cell dynamics requires first generating linearized Laplace-domain transfer functions of all cell internal electrochemical variables of interest. Then, the resulting infinite-dimensional transfer functions can be reduced by various means in order to find an approximate low-dimensional model. These methods include Pade approximation or the Discrete-Time Realization algorithm. In a previous article, Lee and colleagues developed a transfer function of the electrolyte concentration for a porous-electrode pseudo-two-dimensional lithium-ion cell model. Their approach used separation of variables and Sturm–Liouville theory to compute an infinite-series solution to the transfer function, which they then truncated to a finite number of terms for reasons of practicality. Here, we instead use a variation-of-parameters approach to arrive at a different representation of the identical solution that does not require a series expansion. The primary benefits of the new approach are speed of computation of the transfer function and the removal of the requirement to approximate the transfer function by truncating the number of terms evaluated. Results show that the speedup of the new method can be more than 3800.

Ethanol is associated with oxidative stress. Exposure to ethanol during childhood may lead to neurological disorders. Congenital disorders induced by alcohol are mainly caused by an oxidative-inflammatory cascade due to extensive apoptotic neurodegeneration in the brain, particularly in the hippocampus. Simvastatin, which acts as an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA), is widely used to manage cardiovascular diseases. Recently, the neuroprotective effects of simvastatin against nervous system disorders have been introduced. In this study, we examined the protective effects of simvastatin on ethanol-related neurotoxicity in the hippocampus of rat pups. Ethanol (5.27 g/kg) in a milk solution (27.8 mL/kg) was administered to male rat pups via intragastric intubation at 2-10 days after birth. Also, 10 and 20 mg/kg of simvastatin were injected to the animals. By using Morris water maze task, the hippocampus-dependent memory and spatial learning was evaluated 36 days after birth. An ELISA assay was performed to investigate the antioxidant and anti-inflammatory effects of simvastatin by measuring the levels of tumor necrosis factor-α (TNF-α), and antioxidant enzymes. To assess the expression levels of Iba1 immunohistochemical staining and caspase-3 immunofluorescence staining was performed. The current study demonstrated that administration of simvastatin significantly attenuates spatial memory impairment (P < 0.01) after ethanol neurotoxicity. Also simvastatin could considerably increase the total superoxide dismutaseand glutathione levels (P < 0.01). Moreover, it was associated with a greater reduction in malondialdehyde (P < 0.05) and TNF-α levels, compared to the ethanol group (P < 0.01). Furthermore, in the simvastatin group, the hippocampal level of caspase-3 and the level of Iba1-positive cells, reduced (P < 0.01). This study demonstrated that apoptotic signaling, mediated by the oxidative-inflammatory cascade, could be inhibited by simvastatin in rat pups with ethanol exposure in the postnatal period.

Xuanwei City (formerly known as Xuanwei County) locates in the northeastern of Yunnan Province and is rich in coal, iron, copper and other mines, especially the smoky (bituminous) coal. Unfortunately, the lung cancer morbidity and mortality rates in this region are among China's highest, with a clear upward trend from the mid-1970s to mid-2000s. In 2004-2005, the crude death rate of lung cancer was 91.3 per 100,000 in the whole Xuanwei City, while that for Laibin Town in this city was 241.14 per 100,000. The epidemiologic distribution (clustering patterns by population, time, and space) of lung cancer in Xuanwei has some special features, e.g., high incidence in rural areas, high incidence in females, and an early age peak in lung cancer deaths. The main factor that associates with a high rate of lung cancer incidence was found to be indoor air pollution caused by the indoor burning of smoky coal. To a certain extent, genetic defects are also associated with the high incidence of lung cancer in Xuanwei. Taken together, lung cancer in this smoky coal combustion region is a unique model for environmental factor-related human cancer, and the current studies indicate that abandoning the use of smoky coal is the key to diminish lung cancer morbidity and mortality.

Alcoholism is associated with a higher incidence of smoking. In addition to the stimulatory effects of both ethanol and nicotine on the mesolimbic reward pathway, nicotine's ability to counteract some of the adverse effects of ethanol (e.g. ataxia) may be a powerful incentive for alcohol consumers to increase their tobacco (nicotine) intake. The cerebellum is believed to play an important role in ethanol-induced ataxia. In this study, we sought to test the hypothesis that nicotine would protect against toxic effects of ethanol in primary cultures of cerebellar granule cells. Moreover, it was postulated that the effects of nicotine would be mediated through nicotinic receptors. Primary cultures of cerebellar granule cells were prepared from 20-day embryos obtained from timed-pregnant Sprague Dawley rats. Cells were cultured for 10 days and were then exposed for 3 days to various concentrations of ethanol with and without pretreatment with nicotine and nicotinic antagonists. Cellular toxicity was evaluated by measuring the lactate dehydrogenase level. Administration of ethanol (10-100 mM) resulted in a dose-dependent toxicity. Pretreatment with nicotine 1-20 micro M resulted in a dose-dependent protection against ethanol-induced toxicity. The effects of nicotine were blocked by pretreatment with nicotinic antagonists such as mecamylamine 1-20 micro M, dihydro-beta-erythroidine 1.0 nM-1.0 micro M and methyllycaconitine 5 nM-5 micro M in a dose-dependent manner. Thus, ethanol-induced cytotoxicity in primary cultures of cerebellar granule cells is blocked by pretreatment with nicotine. The effects of nicotine, in turn, may be blocked by nicotinic antagonists, implicating both high and low affinity nicotinic receptors in mediating the actions of nicotine. The exact mechanism of ethanol-induced toxicity and/or neuroprotection through activation of nicotinic receptors in this paradigm remains to be elucidated. The neuroprotective effect of nicotine against ethanol-induced toxicity in cerebellar neurons may be a contributing factor to the high incidence of smoking among alcoholics.

Background: Most of the studies of alcoholic liver disease use models in which animals undergo involuntary administration of high amounts of ethanol and consume diets that are often high in polyunsaturated fatty acids. The objectives of this study were (1) to evaluate whether cynomolgus monkeys (Macaca fascicularis) drinking ethanol voluntarily and consuming a diet with moderate amounts of lipid would demonstrate any indices of alcoholic liver disease past the fatty liver stage and (2) to determine whether these alterations were accompanied by oxidative stress.Methods: Six adult male and 6 adult female cynomolgus monkeys were allowed to consume ethanol voluntarily for 18 to 19 months. Additional monkeys were maintained on the same consumption protocol, but were not provided with ethanol. During the course of the study, liver biopsy samples were monitored for lipid deposition and inflammation, serum for levels of liver enzymes, and urine for concentrations of the isoprostane (IsoP) metabolite, 2,3‐dinor‐5,6‐dihydro‐15‐F2t‐IsoP, a biomarker for oxidative stress. Liver mitochondria were monitored for respiratory control and liver for concentrations of neutral lipids, adenine nucleotides, esterified F2 isoprostanes, oxidized proteins, 4‐hydroxynonenal (HNE)‐protein adducts, and protein levels of cytochrome P‐450 2E1 and 3A4.Results: Ethanol consumption ranged from 0.9 to 4.05 g/kg/d over the period of the study. Serum levels of aspartate amino transferase were elevated in heavy‐consuming animals compared with those in ethanol‐naïve or moderate drinkers. Many of the ethanol consumers developed fatty liver and most showed loci of inflammation. Both hepatic energy charge and phosphorylation potential were decreased and NADH‐linked respiration was slightly, but significantly depressed in coupled mitochondria as a result of heavy ethanol consumption. The urinary concentrations of 2,3‐dinor‐5,6‐dihydro‐15‐F2t‐IsoP increased as high as 33‐fold over that observed in ethanol‐abstinent animals. Liver cytochrome P‐450 2E1 concentrations increased in ethanol consumers, but there were no ethanol‐elicited increases in hepatic concentrations of the esterified F2 isoprostanes, oxidized proteins, or HNE‐protein adducts.Conclusion: Our studies show that cynomolgus monkeys undergoing voluntary ethanol consumption for 1.5 years exhibit many of the features observed in the early stages of human alcoholic liver disease. Ethanol‐elicited fatty liver, inflammation, and elevated serum aspartate amino transferase were evident with a diet that contained modest amounts of polyunsaturated lipids. The dramatic increases in urinary IsoP demonstrated that the animals were being subjected to significant oxidative stress that correlated with their level of ethanol consumption.

The association between alcohol and blood glucose levels, and whether it is modified by other variables, was examined in a cross-sectional survey of 5518 staff aged 40-65 years at worksites in Auckland and Tokoroa, New Zealand. Diabetes was determined by oral glucose-tolerance tests using 1999 WHO criteria. Usual alcohol intake in the previous 3 months, measured by food frequency questionnaire, was related positively with fasting triglycerides and high-density-lipoprotein (HDL)-cholesterol, and unrelated with fasting glucose, but had an approximate U-shaped relationship with 2-h glucose, which varied from an adjusted mean (S.E.) of 5.62 (0.08) mmol/l in non-drinkers, down to 5.34 (0.08) mmol/l in light alcohol drinkers (alcohol or =20 g per day). Adjusting further for triglycerides increased the mean difference in 2-h glucose for all drinking categories compared with non-drinkers, particularly for heavy drinkers (> or =20 g per day), from -0.22 (S.E. = 0.10) to -0.37 (0.10) mmol/l. The confounding effect of triglycerides suggests alcohol may affect the diabetes risk by a mechanism related to the triglyceride metabolism, which in heavy drinkers may counteract the protective effect of improved insulin sensitivity, resulting in the U-shaped relationship between alcohol and diabetes described in previous studies.

In developing an algal treatment system, selenium (Se) removal efficiency by Chlorella vulgaris was evaluated under various conditions such as Se concentration, algal density, temperature and pH. A maximum removal efficiency plateau of ∼90% was observed between 1000-3000 μg Se/L while the tolerance of Se toxicity was found at 6000 μg Se/L. C. vulgaris of 0.75 g DW/L showed the highest removal efficiency (84%), and volatilization was dominant below 1.37 g DW/L. Se volatilization was two times higher at 25 °C than at 20 °C in the first 24 h. Moreover, the highest removal efficiency (77%) was obtained at pH 8.0, compared to 66.5% at pH 6.5 and 40% at pH 10.0. To prevent ecotoxicity, Se laden algae were further burned to ashes or filtered out by Anodonta woodiana. After burning, biomass Se was reduced by 99%, with organo-Se entirely converted into inorganic Se, lowering Se bioavailability. A. woodiana removed 54% of Se in 24 h, leading to Se bioaccumulation in soft tissues, which may serve as dietary Se supplements for human health. Our results suggest the cleanup of Se-contaminated water from either agricultural runoff or industrial discharge could be achieved using an algal treatment system with minimum potential ecotoxicity.

Indoor air pollution in developing countries is a public health problem deserving of urgent attention. The aim of this study was to assess indoor second‐hand smoke (SHS) exposure via PM2.5 (fine particles with diameter ≤ 2.5 μm) level measurements in several public venues in Kuwait. The PM2.5 mean, median, and interquartile range (IQR) values for nonsmoking areas were; respectively, 28, 24, 32 μg/m3 while the corresponding values for smoking areas were 274, 222, 288 μg/m3 in the absence of water pipe usage and 1434, 1001, 964 μg/m3 in the presence of water pipes, respectively. Differences among the three tested venues (nonsmoking, smoking with and without water pipes) were statistically significant (F = 330.7, P < 0.001). The air quality index (AQI) results showed that nonsmoking areas were mostly classified as either “Good” or “Moderate” whereas the classification in smoking areas varied between “Moderate” to “Hazardous.” Adverse health outcomes from exposure to PM2.5 were also evaluated. The estimated lifetime lung cancer and cardiopulmonary risks in nonsmoking area were 4 × 10−3 and 3 × 10−3, respectively. In smoking areas, the risks were more than sixfold and 30‐fold increases of cancer and cardiopulmonary relative to nonsmoking areas without and with water pipes, respectively. In smoking venues, the relative ratio values were 1.26 and 1.16 with no water pipe and 1.86 and 1.51 when water pipe usage was observed, for lung cancer and cardiopulmonary mortality, respectively. These values reveal that people, especially the young and elderly, occupying or visiting these venues are susceptible to lung cancer and cardiopulmonary mortality. © 2018 American Institute of Chemical Engineers Environ Prog, 38:e13096, 2019