The role of a nuclear protein, histone H1, on signalling pathways for the maturation of dendritic cells.

We have demonstrated previously that liver allograft tolerance is associated with the immunosuppressive activity of anti-histone H1 autoreactive antibodies induced in the serum of liver transplantation. Furthermore, we and others have shown that nuclear proteins such as histone H1 and high mobility group box 1 play an important role in maturation of dendritic cells (DCs), although the precise mechanisms are still unknown. In the present study, we focus upon the significance of histone H1 on DCs in terms of the intracellular signalling pathway of DCs. Our immunostaining and immunoblot studies demonstrated that histone H1 was detected in cytoplasm and culture supernatants upon the activation of DCs. Histone H1 blockage by anti-histone H1 antibody down-regulated the intracellular activation of mitogen-activated protein kinases (MAPKs) (p38) and IkappaBalpha of DCs, and inhibited DC activity in the proliferation of CD4+ T cells. On the other hand, the addition of histone H1 without endotoxin stimulation up-regulated major histocompatibility complex class II, the CD80 and CD86 surface markers of DCs and the activation of MAPKs (p38 and extracellular-regulated kinase 1/2) and IkappaBalpha. These results suggest that the translocation of histone H1 from nuclei to cytoplasm and the release of their own histone H1 are necessary for the maturation of DCs and the activation for T lymphocytes.

UV treatments on the physicochemical properties of tilapia skin and pig skin gelatin.

Tilapia skin gelatin, pig skin gelatin, and their mousse premixes were exposed to UV irradiation for 103, 206, and 309 kJ/cm(2). All samples after 309 kJ/cm(2) exposure exhibited a significant increase in gel strength, gel forming ability as well as viscosity of solutions. It was shown that UV treatment could also improve the pig skin gelatin foam stability and foam formation ability compared to those of tilapia skin gelatin. Nevertheless, the panelists gave the lowest scores to mousse made with 309 kJ/cm(2) UV-irradiated premix mousse pig skin gelatin. Tilapia skin gelatin could be used as a substitute ingredient for premix mousse made from pig skin gelatin.

Gender differences in tobacco use in Africa, Asia, the Pacific, and Latin America.

This paper reviews historical, anthropological and contemporary survey data concerning gender differences in tobacco use in Africa, Asia, the Pacific, and Latin America. In many cultural groups in these regions, tobacco use has been substantially more common among men than among women. In some groups, tobacco use has been about equally common for both sexes. No evidence was found of any group in which tobacco use has been substantially more common among women. The widespread pattern of greater tobacco use by men appears to be linked to general features of sex roles. For example, men have often had greater social power than women, and this has been expressed in greater restrictions on women's behavior, including social prohibitions against women's smoking. These social prohibitions against women's smoking have strongly inhibited women's tobacco use and thus have been a major cause of gender differences in tobacco use. Gender differences in tobacco use have varied in magnitude, depending on the type of tobacco use and the particular cultural group, age group and historical period considered. Causes of the variation in gender differences in tobacco use include variation in women's status and variation in the social significance and benefits attributed to particular types of tobacco use in different cultures. Contact with Western cultures appears to have increased or decreased gender differences in smoking, depending on the specific circumstances. The patterns of gender differences in tobacco use in non-Western societies are similar in many ways to the patterns observed in Western societies, but there are several important differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Ischemic reperfusion injury-induced oxidative stress and pro-inflammatory mediators in liver transplantation recipients.

OBJECTIVE: Liver ischemic reperfusion injury is harmful to transplant recipients, and is associated with postoperative morbidity and mortality. Our study was designed to investigate the oxidative stress and pro-inflammatory mediators in liver transplant recipients. METHODS: We prospectively analyzed 14 recipients who underwent liver transplantation by measuring their blood levels of malondialdehyde (MDA) and cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6, at nine time points perioperatively. We also evaluated the correlations between oxidative stress (MDA levels) and the characteristics of the recipient or the donated graft. RESULTS: These parameters significantly increased from 1 minute before reperfusion, and the values peaked within 3 to 30 minutes after reperfusion. On the time point at 5 minutes after reperfusion, the MDA levels which were the highest in the recipients correlated with the values of preoperative direct/and total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), model for end-stage liver disease (MELD) score, international normalized ratio (INR), and surgical blood loss. CONCLUSION: The levels of MDA, TNF-α, IL-1ß, and IL-6 greatly increased with the ischemic reperfusion insult. Recipients with higher values of preoperative direct/and total bilirubin, AST, ALT, MELD score, INR, and surgical blood loss tended to have higher levels of MDA and may suffer more injury from this insult.

The ratio of plasma interleukin-18 is a sensitive biomarker for acute kidney injury after liver transplantation.

BACKGROUND: Acute kidney injury (AKI) is common after liver transplantation (OLT) and is associated with high morbidity and mortality. Previous studies have shown that interleukin-18 (IL-18) levels are associated with AKI. The purpose of this study was to determine whether plasma IL-18 levels were early predictors for AKI after liver transplantation. METHODS: Plasma samples were obtained from 26 patients who underwent OLT at induction of anesthesia (T1), 1 hour after the surgical incision (T2), the time of reperfusion (T3), as well as 1 (T4), 2 (T5), and 4 hours (T6) after reperfusion. Samples were also obtained at 24 hours after surgery (T7). The AKI criteria were taken according to the Acute Kidney Injury Network criteria. RESULTS: Twelve patients (46%) developed AKI after OLT. The area under the receiver operating curve of plasma IL-18 concentrations (T4/T1) to predict AKI occurrence was 0.842 at T5, 0.905 at T6, 0.726 at T7, and 0.726 at T5 to T7. CONCLUSION: Plasma IL-18 concentrations taken 1 hour after reperfusion were predictive of AKI. Therefore, changing IL-18 ratio may be an early predictor for AKI after OLT.

Recent advances in pharmacokinetic applications of capillary electrophoresis.

This article reviews recent capillary electrophoresis (CE)-based assays which were published for pharmacokinetic studies. Both the advantages and disadvantages of these CE-based assays are discussed based on their feasibility and the significance towards the better understanding of pharmacokinetics. In addition, as a future outlook, novel assays such as immunoaffinity CE and chip-based CE for analyzing drugs in biological fluids are summarized in view of their potential for pharmacokinetic applications.

Plastic microchip electrophoresis for genetic screening: the analysis of polymerase chain reactions products of fragile X (CGG)n alleles.

Clinical screening of abnormal chromosomes associated with fragile X syndrome (FXS) demands a high-throughput method including DNA sizing and detection of the amplified products. This study is to explore the use of polymer microchip electrophoresis for the analysis of polymerase chain reaction (PCR) products of fragile X (CGG)n alleles to facilitate a fast exclusion test of FXS. The sequences flanking the CGG-repeat of FMR1 gene was amplified by betaine-PCR and the amplified products were desalted and then analyzed by microchips which were fabricated on poly(methyl methacrylate) (PMMA) substrate. The PCR bands with more than six CGG-repeats in difference could be clearly distinguished in less than 3 min by microchip electrophoresis with a separation length of 6 cm. It was found that the signal was greatly enhanced with the use of both covalent (Cy5) and intercalating dye (TORRO-3), which has never been demonstrated before. We tested the method by reanalysis of twelve samples from males and six samples from females. For female samples with less than six repeat differences, Southern blotting method was performed to confirm or exclude the findings from microchips. It was found that the test results from all male and female samples show a 100% correlation between the microchip electrophoresis and the existing methods.

Effect of vitamin E on rat hepatic cytochrome P-450 activity.

Hepatic cytochrome P-450 activity has been shown to be affected by various dietary factors including vitamin E. However, reports of the effect of dietary vitamin E on cytochrome P-450 activity have been inconsistent. The aim of the present study was to investigate the influence of dietary vitamin E on rat hepatic cytochrome P-450 activity. Three groups of six male weanling Sprague-Dawley rats were fed semipurified diets containing 0, 100, or 1,500 ppm vitamin E for eight weeks. Vitamin E was given in the form of alpha-tocopheryl acetate. Dietary vitamin E significantly affected liver vitamin E content (p < 0.05) but had no effect on rat hepatic total P-450 content, N-nitrosodimethylamine demethylase, and NADPH-cytochrome-P-450 reductase activities. Hepatic pentoxyresorufin O-dealkylase and glutathione S-transferase activities were significantly greater in rats fed 100 and 1,500 ppm vitamin E than in rats fed no vitamin E (p < 0.05). Dietary vitamin E induced changes in hepatic phospholipid fatty acid composition. Hepatic phospholipid linoleate was significantly greater in rats fed 0 and 1,500 ppm vitamin E than in rats fed 100 ppm vitamin E (p < 0.05). Hepatic phospholipid eicosapentaenoate was increased significantly by dietary vitamin E (p < 0.05). Hepatic thiobarbituric acid-reactive substance was significantly greater in rats fed no vitamin E than in rats fed 100 and 1,500 ppm vitamin E (p < 0.05). The results suggest that vitamin E may influence cytochrome P-450 IIB1 enzyme activity and may affect hepatic phospholipid fatty acid composition.

alpha-Tocopherol acetate supplementation enhances rat hepatic cytochrome PROD activity in the presence of phenobarbital induction.

Hepatic cytochrome P-450 enzymes play important roles in bioactivation of chemical carcinogens, biotransformation of many endogenous compounds, and detoxification of numerous xenobiotics. These enzyme activities have been shown to be regulated by various dietary factors. In our previous study, hepatic cytochrome pentoxyresorufin O-dealkylase (PROD) activity was decreased in rats fed an alpha-tocopherol acetate-deficient diet compared with rats fed alpha-tocopherol acetate-adequate or -supplemented diets. The objective of the present study was to investigate whether the modulatory effect of dietary alpha-tocopherol acetate on hepatic cytochrome PROD activity is influenced by the presence of phenobarbital. Weanling male Sprague-Dawley rats were fed the AIN-76 diet for four days, fasted for two days, then fed semipurified diets that were alpha-tocopherol acetate deficient, adequate, or supplemented with 5 and 15 g/kg alpha-tocopherol acetate for four days. Liver and plasma alpha-tocopherol concentrations were dose dependently regulated by dietary alpha-tocopherol acetate level. Inhibition of lipid peroxidation by dietary alpha-tocopherol acetate was dose dependent. Hepatic total cytochrome P-450 content was significantly greater in rats fed diets supplemented with 5 and 15 g/kg alpha-tocopherol acetate than in rats fed an alpha-tocopherol-adequate diet (p < 0.05). Hepatic cytochrome PROD activity was significantly greater in rats fed diets supplemented with 5 and 15 g/kg alpha-tocopherol acetate than in rats fed alpha-tocopherol acetate-deficient and -adequate diets (p < 0.05). These results suggest that, in the presence of phenobarbital, dietary alpha-tocopherol acetate efficiently affects tissue alpha-tocopherol levels and inhibits lipid peroxidation and that diets supplemented with 5 or 15 g/kg alpha-tocopherol acetate enhance hepatic cytochrome PROD activity compared with alpha-tocopherol acetate-deficient or -adequate diets.

A disposable poly(methylmethacrylate)-based microfluidic module for protein identification by nanoelectrospray ionization-tandem mass spectrometry.

The design, fabrication, and analytical use of a poly(methylmethacrylate) (PMMA)-based microfluidic module for nanoelectrospray ionization-tandem mass spectrometry (nano-ESI-MS/MS) were described. The microfluidic module can be mass-produced at low costs and used as a disposable device to generate nano-ESI-MS/MS signals for protein identification from low amounts of protein samples. Compared with commercially available nanospray capillary tips, the module gave comparable signal quality and also offered advantages in convenience and easiness of operation, permitting repeated usage, and disposability.

Effect of dietary vitamin E on antioxidant status and antioxidant enzyme activities in Sprague-Dawley rats.

The effect of dietary vitamin E on plasma, red blood cells (RBC), hepatic antioxidant status, and antioxidant enzyme activities was investigated. Three groups of six Sprague-Dawley rats were fed 0, 100, or 1,500 ppm vitamin E for eight weeks. Plasma alpha-tocopherol level was increased significantly by increasing dietary vitamin E (p < 0.05). Plasma lipid peroxidation (thiobarbituric acid-reactive substances) stimulation by 1 mM t-butyl hydroperoxide was correlated with dietary vitamin E level and was significantly greater in rats fed no vitamin E than in rats fed 100 or 1,500 ppm vitamin E (p < 0.05). RBC reduced glutathione (GSH) level was positively correlated with dietary vitamin E and was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed 0 or 100 ppm vitamin E (p < 0.05). RBC oxidized glutathione was negatively correlated with dietary vitamin E. GSH redox status was expressed as the GSH-to-total GSH ratio; the ratio was also positively correlated with dietary vitamin E and was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed no vitamin E (p < 0.05). For antioxidant enzymes, superoxide dismutase activity in hepatic cytosolic fraction was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed 100 ppm vitamin E. Hepatic GSH reductase activity was significantly greater in rats fed 100 ppm vitamin E than in rats fed no vitamin E (p < 0.05). Dietary vitamin E had no effect on plasma vitamin C and protein thiol levels. In the systems studied, results indicated that dietary vitamin E selectively influences plasma vitamin E level, RBC GSH status, and hepatic cytosolic superoxide dismutase and GSH reductase activities.