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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.

A multivariate analysis of dimensions of problem drinking and their stability across time is conducted through a series of confirmatory factor analyses (as opposed to exploratory factor analyses used in previous studies), using self-report data from a longitudinal sample of adolescents and youth. Analyses are performed separately by age and gender. Results indicate that traditional measures of problem drinking represent at least two distinct dimensions--intensity of use and use-related problems--rather than a unitary construct for adolescent males and females. The results also suggest that dimensions of problem drinking remain relatively stable from 15 to 21 years of age, except that alcohol-related problems are unstable for males from 15 to 18 years of age.

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.

Tumor necrosis factor-alpha (TNF-alpha) production is a critical factor in the pathogenesis of alcoholic liver injury. Both oxidative stress and endotoxin have been implicated in the process of alcohol-induced TNF-alpha production. However, a cause-and-effect relationship between these factors has not been fully defined. The present study was undertaken to determine the mediators of acute alcohol-induced TNF-alpha production using a mouse model of acute alcohol hepatotoxicity. Alcohol administration via gavage at a dose of 6 g/kg to 129/Sv mice induced hepatic TNF-alpha production in Kupffer cells as demonstrated by measuring protein levels, immunohistochemical localization, and mRNA expression. Alcohol intoxication caused liver injury in association with increases in plasma endotoxin and hepatic lipid peroxidation. Treatment with an endotoxin neutralizing protein significantly suppressed alcohol-induced elevation of plasma endotoxin, hepatic lipid peroxidation, and inhibited TNF-alpha production. Treatment with antioxidants, N-ACETYL-L-CYSTEINE, or dimethylsulfoxide, failed to attenuate plasma endotoxin elevation, but significantly inhibited alcohol-induced hepatic lipid peroxidation, TNF-alpha production and steatosis. All treatments prevented alcohol-induced necrotic cell death in the liver. This study thus systemically dissected the relationship among plasma endotoxin elevation, hepatic oxidative stress, and TNF-alpha production following acute alcohol administration, and the results demonstrate that oxidative stress mediates endotoxin-induced hepatic TNF-alpha production in acute alcohol intoxication.

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.

To determine the relationship among helmet use, alcohol use, and ethnicity in people killed on motorcycles.Retrospective review of all motorcycle fatalities in New Mexico from 1984 through 1988.Office of the Medical Investigator, State of New Mexico.All decedents of motorcycle crashes in New Mexico from 1984 through 1988.Review of all autopsies, medical investigator reports, traffic fatality reports, and toxicological studies on fatally injured motorcyclists.Nine of the helmeted drivers (18%) were legally intoxicated compared with 67 of the nonhelmeted drivers (51%) (chi 2 = 15.7, P less than .0001); 42 of the white nonHispanic decedents (37%), ten of Hispanic decedents (12%), and none of the Native-American decedents were wearing helmets. The head and neck region was the most severely injured body region in 42 of the nonhelmeted cases (84%) and in eight of the helmeted cases (50%) (Fisher's exact test, P less than .02).There is an association between nonuse of helmets and alcohol intoxication in fatally injured motorcyclists in New Mexico. Strategies for preventing motorcycle fatalities should address alcohol abuse and ethnicity in conjunction with helmet use.

Previous studies on the adverse effects of perinatal exposure to ethanol (EtOH) on the developing visual system mainly focused on retinal and optic nerve morphology. The aim of the present study was to investigate whether earlier reported retinal and optic nerve changes are accompanied by anomalies in eye-specific fiber segregation in the dorsal lateral geniculate nucleus (dLGN). C57BL/6 mice pups were exposed to ethanol by intragastric intubation at either 3 or 4 g/kg from postnatal days (PD) 3-10, the third trimester equivalent to human gestation. Control (C) and intubation control (IC) groups not exposed to ethanol were included. On PD9, retinogeniculate projections were labeled by intraocular microinjections of cholera toxin-β (CTB) either conjugated to Alexa 488 (green) or 594 (red) administrated to the left and right eye, respectively. Pups were sacrificed 24 h after the last CTB injection. The results showed that ethanol exposure decreased the total number of dLGN neurons and significantly reduced the total dLGN projection as well as the contralateral and ipsilateral projection areas.