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The generally accepted hypothesis for the pathogenesis of alcoholic liver disease (ALD) is the two-hit model, which proposes that fat accumulation in the liver increases the sensitivity of the liver to a second hit that leads to inflammatory liver cell damage. In this study we evaluated the effects of Magnolia officinalis (MO), which contains honokiol and magnolol as the primary pharmacological components, to eradicate fatty liver in rats fed an ethanol diet. In vitro studies showed that MO was able to protect RAW 264.7 cells from ethanol-induced production of tumor necrosis factor-alpha, reactive oxygen species, and superoxide anion radicals; the activation of NADPH oxidase; and subsequent cell death. We also investigated the therapeutic effects of MO on alcoholic fatty liver in Lieber-DeCarli ethanol diet-fed rats. MO treatment of the rats for the last 2 weeks of ethanol feeding completely reversed all the serum, hepatic parameters, and fatty liver changes. The increased maturation of sterol regulatory element-binding protein-1c in the liver by ethanol treatment was completely inhibited by treatment with MO. Therefore, MO may be a promising candidate for development as a therapeutic agent for ALD.

We previously developed a model for projection of heat-related mortality attributable to climate change. The objective of this paper is to improve the fit and precision of and examine the robustness of the model.We obtained daily data for number of deaths and maximum temperature from respective governmental organizations of Japan, Korea, Taiwan, the USA, and European countries. For future projection, we used the Bergen climate model 2 (BCM2) general circulation model, the Special Report on Emissions Scenarios (SRES) A1B socioeconomic scenario, and the mortality projection for the 65+-year-old age group developed by the World Health Organization (WHO). The heat-related excess mortality was defined as follows: The temperature-mortality relation forms a V-shaped curve, and the temperature at which mortality becomes lowest is called the optimum temperature (OT). The difference in mortality between the OT and a temperature beyond the OT is the excess mortality. To develop the model for projection, we used Japanese 47-prefecture data from 1972 to 2008. Using a distributed lag nonlinear model (two-dimensional nonparametric regression of temperature and its lag effect), we included the lag effect of temperature up to 15 days, and created a risk function curve on which the projection is based. As an example, we perform a future projection using the above-mentioned risk function. In the projection, we used 1961-1990 temperature as the baseline, and temperatures in the 2030s and 2050s were projected using the BCM2 global circulation model, SRES A1B scenario, and WHO-provided annual mortality. Here, we used the "counterfactual method" to evaluate the climate change impact; For example, baseline temperature and 2030 mortality were used to determine the baseline excess, and compared with the 2030 excess, for which we used 2030 temperature and 2030 mortality. In terms of adaptation to warmer climate, we assumed 0 % adaptation when the OT as of the current climate is used and 100 % adaptation when the OT as of the future climate is used. The midpoint of the OTs of the two types of adaptation was set to be the OT for 50 % adaptation.We calculated heat-related excess mortality for 2030 and 2050.Our new model is considered to be better fit, and more precise and robust compared with the previous model.

Abstract This work investigates a pattern recognition-based diagnosis approach as an application of the Hamming neural network to the identification of suitable fuel cell model parameters, which aim to diagnose state-of-health (SOH) for a polymer electrolyte membrane (PEM) fuel cell. The fuel cell output voltage (FCOV) patterns of the 20 PEM fuel cells were measured, together with the model parameters, as representative patterns. Through statistical analysis of the FCOV patterns for 20 single cells, the Hamming neural network is applied for identification of the representative FCOV pattern that matches most closely of the pattern of the arbitrary cell to be measured. Considering the equivalent circuit fuel cell model, the purpose is to select a representative loss ΔRd, defined as the sum of two losses (activation and concentration losses). Consequently, the selected cell’s ΔRd is properly applied to diagnose SOH of an arbitrary cell through the comparison with those of fully fresh and aged cells with the minimum and maximum of the ΔRd in experimental cell group, respectively. This avoids the need for repeated parameter measurement. Therefore, these results could lead to interesting perspectives for diagnostic fuel cell SOH.

The effects of ginsenosides Rg3(R), Rg3(S) and Rg5/Rk1 (a mixture of Rg5 and Rk1, 1:1, w/w), which are components isolated from processed Panax ginseng C.A. Meyer (Araliaceae), on memory dysfunction were examined in mice using a passive avoidance test. The ginsenosides Rg3(R), Rg3(S) or Rg5/Rk1, when orally administered for 4 days, significantly ameliorated the memory impairment induced by the single oral administration of ethanol. The memory impairment induced by the intraperitoneal injection of scopolamine was also significantly recovered by ginsenosides Rg3(S) and Rg5/Rk1. Among the three ginsenosides tested in this study, Rg5/Rk1 enhanced the memory function of mice most effectively in both the ethanoland scopolamine-induced amnesia models. Moreover, the latency period of the Rg5/Rk1-treated mice was 1.2 times longer than that of the control (no amnesia) group in both models, implying that Rg5/Rk1 may also exert beneficial effects in the normal brain. We also evaluated the effects of these ginsenosides on the excitotoxic and oxidative stress-induced neuronal cell damage in primary cultured rat cortical cells. The excitotoxicity induced by glutamate or N-methyl-D-aspartate (NMDA) was dramatically inhibited by the three ginsenosides. Rg3(S) and Rg5/Rk1 exhibited a more potent inhibition of excitotoxicity than did Rg3(R). In contrast, these ginsenosides were all ineffective against the H2O2- or xanthine/xanthine oxidase-induced oxidative neuronal damage. Taken together, these results indicate that ginsenosides Rg3(S) and Rg5/Rk1 significantly reversed the memory dysfunction induced by ethanol or scopolamine, and their neuroprotective actions against excitotoxicity may be attributed to their memory enhancing effects.

Performance of a polymer electrolyte membrane fuel cell with a Pd cathode catalyst was systemically investigated in this study. The Pd catalyst was directly formed on a gas diffusion layer by using electrodeposition (Pd/GDL). The electrodeposition formed aggregates of Pd nanoparticles on a gas diffusion layer with the preferred orientation of Pd(111) and Pd(200). In addition, the Pd aggregates mainly formed on the top surface of the gas diffusion layer. The membrane electrode assembly was fabricated with Pd/GDL as the cathode. The performance of the membrane electrode assembly was investigated by varying hot pressing parameters and back pressures, and the operating condition for the polymer electrolyte membrane fuel cell was optimized. Notably, introducing back pressure increased operating current density at 0.6 V by up to 45%. Durability of the membrane electrode assembly was also examined. Negligible deterioration of surface morphology of the Pd catalyst was observed even after accelerated stress testing, except for a slight increase in particle size. The results indicate that deterioration of the Pd cathode catalyst was not a major factor affecting overall single-cell performance degradation.

We induced experimental renal arterial embolization with the radiopaque solution of ethanol and iodized oil (Lipiodol) in 35 rabbits to evaluate the capability of the mixture to induce renal ablation. Serial renal angiography and plain abdominal radiography were performed immediately, one week and two weeks after embolization. Neither pure Lipiodol nor a 50% ethanol solution caused renal embolization. However, infusion of 50% and 75% ethanol-Lipiodol solutions resulted in embolization equal to that caused by absolute ethanol. The 50% ethanol-Lipiodol solution was so radiopaque that we could easily observe the embolization process during fluoroscopy. Renal arterial embolization with the 50% ethanol-Lipiodol solution was successful in three patients with hypernephroma. Our results suggest that a 50% ethanol-Lipiodol solution is radiopaque and an effective agent for renal arterial embolization.

Aloe contains abundant aloin, a C-glycoside derivative of anthraquinone. Based on recent reports indicating that the water extract of Aloe enhances the ethanol oxidation rate and also that quinones, in general, have a functional role in elevating the alcohol oxidation rate in vivo, we have attempted to identify the quinone derivative contained in Aloe that could increase the alcohol oxidation rate. Upon oral administration of aloin (300 mg/kg) given 12 hr prior to the administration of alcohol (3.0 g/kg), the blood alcohol area under the curve (AUC) was found to be decreased significantly (by 40%). This was supported by increases in the rates of blood alcohol elimination and the disappearance of alcohol from the body by 45 and 50%, respectively. Analysis of hepatic triglyceride (TG) levels revealed that both the ethanol and the aloin treatment alone significantly increased the TG levels in a comparable manner; however, the level obtained by the combined treatment of aloin and ethanol was not statistically different from that produced by either treatment alone. The levels of serum L-aspartate:2-oxoglutarate aminotransferase (AST) and L-alanine:2-oxoglutarate aminotransferase (ALT) activities were not increased by acute alcohol intoxication, aloin alone, or by the combined treatment of alcohol and aloin. Pretreatments with aloe-emodin, the anthraquinone aglycone of aloin, resulted in a significantly decreased blood alcohol AUC and an increase in the rate of ethanol disappearance. These results suggested that when the aloin localized primarily in the skin of Aloe is ingested, aloe-emodin (the quinone aglycone) may be released, and the released quinone may produce acceleration of the ethanol metabolism rate in vivo.

Purpose: To evaluate the therapeutic effects of topical 8-oxo-2ʹ-deoxyguanosine (8-oxo-dG) on experimental ocular chemical injury models. Methods: We created ocular chemical injury models with 8-week-old BALB/c mice (n = 70) by applying 100% ethanol; the mice were then treated with 8-oxo-dG eye drops 10 and 5 mg/mL and phosphate-buffered saline (PBS) twice daily. After 7 days, clinical findings such as corneal integrity, clarity, and neovascularization were assessed. Histology, immunohistochemistry findings, and inflammatory cytokine levels using real-time polymerase chain reactions in the corneas of the mice were also analyzed. Results: Topical application of 8-oxo-dG eye drops resulted in a significant improvement of epithelial defects and clarity, dose dependently (each P < 0.001). Inflammatory cell infiltration and corneal stromal edema were also decreased in the 8-oxo-dG-treated mice compared with PBS-treated controls, based on hematoxylin and eosin staining. The expressions of F4/80 and neutrophil elastase–positive inflammatory cells and IL-1 and TNF-α cytokine levels were significantly reduced in the 8-oxo-dG group compared with the PBS group (each P < 0.01). Conclusions: Topical 8-oxo-dG application showed an excellent therapeutic effect in ocular chemical injury models by suppressing inflammation.