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Abstract In this study, a multi-phase, two-dimensional model that integrates the bipolar plate (BP) and gas diffusion layer (GDL) interfacial morphology was developed to understand the effects of this interface on mass, charge and heat transport and performance of polymer electrolyte fuel cells (PEFCs). Two different case studies were performed. The first case assumes a perfect contact interface between the BP and GDL, whereas in the second case, the BP|GDL interfacial layer was incorporated as a separate domain based on the measured BP|GDL morphology. In the BP|GDL interface case, the interfacial voids were assumed to be filled with liquid water to investigate the role of the interfacial voids. For both cases, the effects of different current densities on the in-plane temperature, saturation, and oxygen concentration distribution in the GDL were investigated. Simulations indicate that the Ohmic and concentration losses are increased due to the inclusion of the realistic BP|GDL interface. The electrical contact resistance contribution of the BP|GDL interface was predicted to be 3.8 mΩcm 2 . The saturation in the GDL was found to be higher for the BP|GDL interface case, which results in higher concentration losses. The temperature was predicted to be slightly higher for the BP|GDL interface case, which could be attributed to the higher thermal contact resistance due to the fewer contact regions at the interface.

Background:The ventral tegmental area (VTA) is involved in regulating ethanol drinking, and the posterior VTA seems to be a neuroanatomical substrate that mediates the reinforcing effects of ethanol in ethanol‐naïve Wistar and ethanol‐naïve alcohol‐preferring (P) rats. The objective of this study was to test the hypothesis that chronic ethanol drinking increases the sensitivity of the posterior VTA to the reinforcing effects of ethanol.Methods:Two groups of female P rats (one given water as its sole source of fluid and the other given 24‐hr free‐choice access to 15% ethanol and water for at least 8 weeks) were stereotaxically implanted with guide cannulae aimed at the posterior VTA. One week after surgery, rats were placed in standard two‐lever (active and inactive) operant chambers and connected to the microinfusion system. Depression of the active lever produced the infusion of 100 nl of artificial cerebrospinal fluid (CSF) or ethanol. The ethanol‐naïve and chronic ethanol‐drinking groups were assigned to subgroups to receive artificial CSF or 25, 50, 75, or 125 mg/dl of ethanol (n= 6–9/dose/group) to self‐infuse (FR1 schedule) during the 4‐hr sessions given every other day.Results:Compared with the infusions of artificial CSF, the control group reliably (p < 0.05) self‐infused 75 and 125 mg/dl of ethanol but not the lower concentrations. The ethanol‐drinking group had significantly (p < 0.05) higher self‐infusions of 50, 75, and 125 mg/dl of ethanol than artificial CSF during the four acquisition sessions; the number of infusions of all three doses was higher in the ethanol‐drinking group than in the ethanol‐naive group. Both groups decreased responding on the active lever when artificial CSF was substituted for ethanol, and both groups demonstrated robust reinstatement of responding on the active lever when ethanol was restored.Conclusions:Chronic ethanol drinking by P rats increased the sensitivity of the posterior VTA to the reinforcing effects of ethanol.

Alcohol use, binge drinking, and alcohol use disorders have been increasing among older adults in the US population, including adults over 50 as well as adults over 65. Increases in consumption are sharper among women, and among those who use additional substances such as cannabis, and those who are relatively healthy in older adulthood (i.e. those without multimorbidites). This commentary describes these trends as well as provides hypotheses, and the data underlying them, for both supply-side (alcohol marketing and messaging) and demand-side (healthier aging, increased financial stress) potential drivers of these increases. The need for additional resources and focus on older adult drinking is increasingly urgent, as alcohol-attributable deaths escalate among older adults in the United States.

Abstract To elucidate the gas generation mechanism due to electrolyte decomposition in commercial lithium-ion cells after long cycling, we developed a device which can accurately determine the volume of generated gas in the cell. Experiments on LixC6/Li1−xCoO2 cells using electrolytes such as 1 M LiPF6 in propylene carbonate (PC), dimethyl carbonate (DMC), ethyl methyl carbonate (EMC), and diethyl carbonate (DEC) are presented and discussed. In the nominal voltage range (4.2–2.5 V), compositional change due mainly to ester exchange reaction occurs, and gaseous products in the cell are little. Generated gas volume and compositional change in the electrolyte are detected largely in overcharged cells, and we discussed that gas generation due to electrolyte decomposition involves different decomposition reactions in overcharged and overdischarged cells.

Abstract When a lithium ion polymer battery (LiPB) is being cycled, one major cause for degradations is the irreversible side reactions between ions and solvent of electrolyte taking place at the surface of anode particles. SEM analysis of cycled battery cells has revealed that the deposits from the side reactions are dispersed not only on particles, but also between the composite anode and the separator. Thus, the solid electrolyte interface (SEI) becomes thicker and extra deposit layers are formed between composite anode and separator. Also, XPS analysis showed that the deposits are composed of Li 2 CO 3 , which is ionic conductive and electronic nonconductive. Based on the mechanisms and findings, we identified four degradation parameters, including volume fraction of accessible active anode, SEI resistance, resistance of deposit layer and diffusion coefficient of electrolyte, to describe capacity and power fade caused by the side reactions. These degradation parameters have been incorporated into an electrochemical thermal model that has been previously developed. The terminal voltage and capacity of the integrated model are compared with experimental data obtained for up to 300 cycles. Finally, the resistance of the deposit layer calculated by the model is validated against the thickness of the deposit layer measured by SEM.

The development of animal models of human disease greatly enhances our ability to study the pathogenesis, prevention and treatment of a particular disease. With relevance to alcoholic liver disease, the use of animal models allows control of genetic heterogeneity, the route, frequency, amount and type of alcohol consumed, and other variables such as nutritional factors and concomitant viral infection. Many different models have been developed to study the toxic effect of alcohol on a variety of organs, but only those used to study alcoholic liver disease are discussed here in detail.

Abstract The intention of the current flow model is to investigate the significance of bioconvection in stagnation point flow of third grade nanofluid containing motile microorganisms past a radiative stretching cylinder. The impacts of activation energy and stagnation point flow are also considered. In addition the behavior of thermophoresis diffusion and Brownian motion are observed. Nanofluid can be developed by dispersing the nanosized particles into the regular fluid. Nano-sized solid materials for example carbides, grephene, metal and alloyed CNT have been utilized for the preparation of nanofluid. Physically, regular fluids have low thermal proficiency. Therefore, nano-size particles can be utilized to enhance the thermal conductivity of the host fluid. Nanofluids have many features in hybrid power engine, heat transfer, and can be used in cancer therapy and medicine. The formulated system of flow problems are transformed into dimensionless coupled ordinary differential expressions system via appropriate transformation. The systems of converted governing expressions are computed numerically by employing well known bvp4c solver in MATLAB software. The outcomes of emerging physical flow parameters on the velocity profile, volumetric concentration of then nanoparticles, rescaled density of the motile microorganisms and nanofluid temperature are elaborated graphically and numerically. Furthermore, velocity of third-grade fluid intensifies for higher values of third-grade fluid parameter and mixed convection parameter while opposite behavior is detected for buoyancy ratio parameter and mixed convection parameter. Temperature distribution grows for higher estimation of temperature ratio parameter and Biot number. Higher amount of Prandtl number and Lewis number decreases the concentration of nanoparticles. Concentration of microorganisms reduces by growing the values of velocity ratio parameter and bioconvection Lewis number.

The abilities of antacid (Mylanta II), sucralfate, cimetidine, and ranitidine to protect the gastric mucosa against ethanol-induced necrosis were compared in a standardized, experimental rat model. Fasted rats received pretreatment with either saline, Mylanta II, 500 mg/kg of sucralfate, 50 mg/kg of cimetidine, or 50 mg/kg of ranitidine. This was followed one hour later by intragastric administration of 2 ml of 100 percent ethanol. Gastric mucosal injury was assessed four hours after administration of ethanol by quantitation of gross mucosal necrosis, assessment of mucosal histology, and determination of intragastric blood and protein concentrations. Pretreatment with Mylanta II or sucralfate significantly reduced ethanol-induced gastric mucosal necrosis. The protective effect of sucralfate was six to 10 times greater than that of Mylanta II. H2-receptor antagonists increased ethanol-induced gastric mucosal necrosis.

Basal levels of serum thyroid‐stimulating hormone (TSH). T3, T4, free T3 and free T4 were measured in 40 chronic alcoholic men and in 31 normal volunteers. Their serum TSH responses to provocative thyrotropin‐releasing hormone (TRH) stimulation were then examined serially: in chronic alcoholics, every 5 days for a total of 3 studies; in 25 of the normal volunteers, before and 72 hr after daily ingestion of ethanol (2 cc/kg/day). Basal serum TSH levels were increased in the alcoholic men (3.5 ± 0.2 μU/ml) (mean ± SEM) compared to those of the normal controls (1.7 ± 0.1) (p < 0.01). Both basal serum T3 and T4 levels (T3, 0.89 ± 0.10 ng/ml; T4, 7.0 ± 0.4 μg/dl) were reduced in the alcoholic men when compared to those of the normal controls (T3,1.20 ± 0.03 ng/ml; T4, 8.6 ± 0.3 μg/dl) (p < 0.01 and p < 0.05, respectively). Basal serum free T3 levels were reduced in the alcoholic men (169 ± 22 pg/dl) compared to the normal controls (380 ± 18) (p < 0.01). In contrast, basal serum free T4 levels were increased in the alcoholics (4.0 ± 0.2 ng/dl) compared to those of the normal controls (2.9 ± 0.1) (p < 0.01). In response to TRH, the serum TSH levels of the alcoholic men achieved a peak of 13.5 ± 0.9 μU/ml compared to 14.9 ± 0.9 for the normal controls (no significant difference). Despite better nutrition and alcohol abstinence associated with hospitalization for 10 days, no improvement in either the basal levels of TSH, T3, and T4 or the TSH responses to provocative TRH was observed in the alcoholic men studied. In normal volunteers, ethanol had no effect on the basal or TRH‐stimulated levels of serum TSH and thyroid hormones.