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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.

Sphingosine is known to have potent biological activity, including pronounced anti-microbial action in vitro against Candida albicans and some bacteria. Several sphingosine bases are present in stratum corneum at concentrations several orders of magnitude above those in other tissues. Sphingosine forms an undissociated salt with organic sulfates, however, so that the free sphingosine in the epidermis may be inactivated by the cholesterol sulfate known to be present. To investigate this hypothesis, C. albicans was grown in cultures with graded concentrations of sphingosine added in ethanol. In 1% ethanol, 0.1-100 microgram/ml sphingosine completely prevented growth of the organism for 12 h. All cultures eventually entered log-phase growth and reached limiting density at a rate inversely proportional to sphingosine concentration. When sphingosine was added, together with an equimolar amount of cholesterol sulfate, there was no delay in the onset of growth of the yeast and the rate of growth and final density were similar to control cultures. These results demonstrate that natural ratios of cholesterol sulfate neutralize the anti-microbial activity of sphingosine in vitro. In the epidermis, endogenous cholesterol sulfate is hydrolyzed by sterol sulfatase at the skin surface, where the released sphingosine may resist microbial colonization of the stratum corneum. This mechanism for liberating anti-microbial sphingosine base only at the skin surface may protect the viable epidermis against known cytotoxic effects of free sphingosine.

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.

Background and Purpose— Ischemic stroke induces metabolic disarray. A central regulatory site, pyruvate dehydrogeanse complex (PDHC) sits at the cross-roads of 2 fundamental metabolic pathways: aerobic and anaerobic. In this study, we combined ethanol (EtOH) and normobaric oxygen (NBO) to develop a novel treatment to modulate PDHC and its regulatory proteins, namely pyruvate dehydrogenase phosphatase and pyruvate dehydrogenase kinase, leading to improved metabolism and reduced oxidative damage. Methods— Sprague–Dawley rats were subjected to transient (2, 3, or 4 hours) middle cerebral artery occlusion followed by 3- or 24-hour reperfusion, or permanent (28 hours) middle cerebral artery occlusion without reperfusion. At 2 hours after the onset of ischemia, rats received either an intraperitoneal injection of saline, 1 dose of EtOH (1.5 g/kg) for 2- and 3-hour middle cerebral artery occlusion, 2 doses of EtOH (1.5 g/kg followed by 1.0 g/kg in 2 hours) in 4 hours or permanent middle cerebral artery occlusion, and EtOH+95% NBO (at 2 hours after the onset of ischemia for 6 hours) in permanent stroke. Infarct volumes and neurological deficits were examined. Oxidative metabolism and stress were determined by measuring ADP/ATP ratio and reactive oxygen species levels. Protein levels of PDHC, pyruvate dehydrogenase kinase, and pyruvate dehydrogenase phosphatase were assessed. Results— EtOH induced dose-dependent neuroprotection in transient ischemia. Compared to EtOH or NBO alone, NBO+EtOH produced the best outcomes in permanent ischemia. These therapies improved brain oxidative metabolism by decreasing ADP/ATP ratios and reactive oxygen species levels, in association with significantly raised levels of PDHC and pyruvate dehydrogenase phosphatase, as well as decreased pyruvate dehydrogenase kinase. Conclusions— Both EtOH and EtOH+NBO treatments conferred neuroprotection in severe stroke by affecting brain metabolism. The treatment may modulate the damaging cascade of metabolic events by bringing the PDHC activity back to normal metabolic levels.

Objective: To evaluate the effectiveness of extracorporeal shockwave therapy compared with other interventions on pain, grip strength and disability in patients with lateral elbow tendinopathy. Data Sources: MEDLINE, PubMed, CINAHL, EMBASE, PEDro, ScienceDirect, Cochrane Library and clinical trial registries. Review methods: We included randomized controlled trials assessing the effectiveness of extracorporeal shockwave therapy alone or as an additive intervention compared with sham or other interventions. Pain intensity, grip strength and elbow disability were used as primary outcome measures. We assessed methodological quality with the PEDro score and quality of evidence with the GRADE approach. Results: Twenty-seven studies with 1871 patients were finally included. Extracorporeal shockwave therapy reduced pain intensity at mid-term follow-up (standardized mean difference: −1.21, 95% confidence interval:−1.53, −0.89, P < 0.001) and improved grip strength at very short- (mean difference:3.92, 95% confidence interval: 0.91, 6.94, P = 0.01) and short-term follow-up (mean difference:4.87, 95% confidence interval:2.24, 7.50, P < 0.001) compared with sham treatment. However, no clinically significant results were found between comparators in all outcomes and follow-up times. Extracorporeal shockwave therapy presented clinically better compared to Laser in grip strength at short-term (mean difference:3.50, 95% confidence interval:2.40, 4.60, P < 0.001) and ultrasound in pain intensity at very-short-term follow-up (standardized mean difference: −1.54, 95% confidence interval: −2.60, −0.48, P = 0.005). Conclusion: Low to moderate certainty of evidence suggests that there are no clinical benefits of extracorporeal shockwave therapy compared to sham interventions or corticosteroid injections. Based on very-low and moderate certainty of evidence, extracorporeal shockwave therapy outperforms against Laser and ultrasound, respectively. Level of Evidence: Therapy, level 1a.

The mechanism of veisalgia cephalgia or hangover headache is unknown. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache.We used a chronic headache model to examine how pure ethanol produces increased sensitivity for nociceptive behaviors in normally hydrated rats.Ethanol initially decreased sensitivity to mechanical stimuli on the face (analgesia), followed 4 to 6 hours later by inflammatory pain. Inhibiting alcohol dehydrogenase extended the analgesia whereas inhibiting aldehyde dehydrogenase decreased analgesia. Neither treatment had nociceptive effects. Direct administration of acetate increased nociceptive behaviors suggesting that acetate, not acetaldehyde, accumulation results in hangover-like hypersensitivity in our model. Since adenosine accumulation is a result of acetate formation, we administered an adenosine antagonist that blocked hypersensitivity.Our study shows that acetate contributes to hangover headache. These findings provide insight into the mechanism of hangover headache and the mechanism of headache induction.

Many of the premature failures in the PEM fuel cells are attributed to crossover of the reactant gas from pinholes or through-the-thickness flaws in the membranes. The formation of these pinholes is not fully understood, although mechanical stress is often considered one of the major factors in their initiation and/or propagation. This paper reports evidence of pinhole failure from mechanical stress by cycling between wet and dry conditions in a normally built single 50cm2 fuel cell. In an effort to understand the source of the mechanical stress, to quantify the magnitude, and to correlate its role in membrane failure, a membrane stress model based on linear viscoelastic theory was developed. The effects of temperature, water content, and time are accounted for in the membrane stress model. To satisfy the inputs for the membrane model and to characterize the mechanical behavior of the polymer electrolyte membrane, a series of experiments was performed. Using commercially available Nafion® NR111 membrane as a model material, swelling of 15% and shrinkage of 4% were found from a hydration and de-hydration cycle. Data on elastic moduli versus relative humidity showed discontinuity at the vapor and liquid water transition. We also found that creep compliance master curves can be obtained by double-shifting the compliance curves according to the time-temperature-moisture superposition principle, which significantly simplifies the modeling effort. Combining data on hygro-expansion, elastic moduli, and creep compliance data through the membrane stress model, it was found that the de-hydration process induces significant stress in the membrane. Due to fluctuations in fuel cell operating conditions, the membrane and the associated components are subject to mechanical fatigue which may mechanically degrade the membrane of PEM fuel cells and eventually lead to pinhole formation.