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In this study, perceived moral obligations were included in the protection motivation theory (PMT) model to explain people's intentions to participate in climate change mitigation behaviors. Empirical data and structural equation modeling results of a nationwide cross-sectional survey in Taiwan confirmed the higher explanatory power of the moral extension PMT model than that of the original PMT model. As expected, threat and coping appraisal of climate change affect protection motivation. In addition, perceived moral obligation affects protection motivation. This protection motivation enhances the intention to participate in climate change mitigation behaviors. The mediation effect of protection motivation was also verified in the moral extension PMT model. Practical implications and suggestions are proposed for the government and related authorities as well as environmental groups to encourage people to participate in climate change mitigation behaviors.

Marine microalgae have been widely applied in cosmaceuticals, nutraceuticals, and functional foods. In the present study, we first investigated the hepatoprotective effects of peptide purified from microalgae, Isochrysis zhanjiangensis on HepG2 cells alcoholic injury. I. zhanjiangensis was hydrolyzed utilizing chymotrypsin, trypsin, pepsin, and by vitro gastrointestinal digestion. Among hydrolysates, the gastrointestinal hydrolysate showed relatively high free radical scavenging ability preliminarily and was purified with following sequential chromatography methods. The amino acid sequence and molecular mass of the purified peptide from I. zhanjiangensis (PIZ) was identified as Asn-Asp-Ala-Glu-Tyr-Gly-Ile-Cys-Gly-Phe (NDAEYGICGF; MW, 1088.16 Da) via Q-TOF ESI/MS. Additionally, PIZ attenuated ethanol-induced cytotoxicity and inhibited the production of intracellular reactive oxygen species by DCFH-DA assay. Western blot results showed that superoxide dismutase (SOD) and glutathione (GSH) levels up-regulated with PIZ treatment before alcohol exposure while gamma-glutamyltransferase (GGT) protein expression down-regulated. These results provide an opportunity to discover new highly active peptide against alcohol toxicity in HepG2 cells.

Despite a growing understanding of health-related quality of life (HRQOL) and its determinants in hemodialysis (HD) patients, little is known about the effects and interrelationships concerning the perception of autonomy support and basic need satisfaction of HD patients on their HRQOL. Based on self-determination theory (SDT), this study examines whether HD patients' perceived autonomy support from health care practitioners (physicians and nurses) relates to the satisfaction of HD patients' basic needs and in turn influences their HRQOL.A questionnaire was administered to 250 Taiwanese HD patients recruited from multiclinical centers and regional hospitals in northern Taiwan. Structural equation modeling (SEM) analysis was conducted to examine the causal relationships between patient perceptions of autonomy support and HRQOL through basic need satisfaction.The empirical results of SEM indicated that the HD patients' perceived autonomy support increased the satisfaction of their basic needs (autonomy, competency, and relatedness), as expected. The higher degree of basic need satisfaction led to higher HRQOL, as measured by physical and mental component scores.Autonomy support from physicians and nurses contributes to improving HD patients' HRQOL through basic need satisfaction. This indicates that staff caring for patients with severe chronic diseases should offer considerable support for patient autonomy.

In this study, we investigated the molecular epidemiology and evolution of influenza viruses from patients infected during the 2013-2014 influenza season in Beijing. A phylogenetic analysis of the hemagglutinin (HA) and neuraminidase (NA) sequences of influenza A and B viruses from 18 patients (6 A(H1N1)pdm09, 4 H3N2, and 8 influenza B virus) was performed. Among the influenza A viruses, A(H1N1)pdm09 was the dominant subtype, whereas the B/Yamagata lineage was predominant for influenza B. The influenza B HA and NA strains in Beijing were dominated by reassortants derived from the Yamagata lineage and the Victoria lineage, respectively. All six A(H1N1)pdm09 strains fell into the 6B genetic group with amino acid substitutions D97N, S185T, K163Q, and A256T; the four H3N2 strains fell into genetic group 3C.3 with substitutions T128A, R142G, N145S, and V186G, and the eight influenza B strains were categorized into subgroup 3.1 and harbored an N217S mutation. Two new mutations (K180Q and G187E at the Sa and Ca antigenic sites of the H1 segment, respectively), which were not detected during the preceding influenza season, were identified. Mutations N131K, S165I, N181Y, and D212N in HA of influenza B mapped to the 120-loop, 150-loop, 160-loop, and 190-helix, respectively. Our results reveal the molecular epidemiology and phylogenetic characteristics of influenza viruses within a single geographic location and can have implications for vaccination selection in northern China.

Different samples of TRIP (transformation induced plasticity) steel obtained by two different hot-rolling schedules are investigated by using a SEM (scanning electron microscope). The microstructure is characterized by using an OM (optical microscope) for phase distribution and by EBSD (electron backscatter diffraction) for texture and phase mapping. ODF (orientation distribution function) graphs are used to investigate the effect of recrystallization behavior of the hot-deformed austenite on phase transformation during the controlled cooling process. The mechanical behavior is interpreted in terms of the strength of both hard and soft phases, in combination with the quantity, location and transformation kinetics of the mechanically induced martensite (TRIP effect). The results show that more austenite grains exist in the steels obtained at finishing rolling temperature (FRT) of 750 °C, which inherited the deformation structure after the hot-rolling process. The instantaneous n value (ni) of those steels is kept high during a large range of strain before failure, while the tensile strength and total elongation of the steels with respect to the different finishing rolling temperatures do not show any significant differences.

Monocyte adhesion to activated vascular endothelial cells is the critical event in the initiation of atherosclerosis. Adhesion molecules are inflammatory markers, which are upregulated by oxidized low-density lipoprotein (ox-LDL) and play a pivotal role in atherogenesis. In present study, the effect of reinioside C, a major compound of Polygala fallax Hemsl., on adhesion of monocytes to endothelial cells induced by ox-LDL was investigated. The results showed that incubation of endothelial cells with ox-LDL (100 microg/mL) for 24 h markedly increased the expression of ICAM-1 and P-selectin and enhanced the adhesion of monocytes to endothelial cells. Pretreatment with reinioside C (1, 3, or 10 microM) dose-dependently decreased ox-LDL-induced upregulation of expression of ICAM-1 and P-selectin and the enhanced adhesion of monocytes to endothelial cells. To determine the role of NADPH oxidase/reactive oxygen species (ROS)/nuclear factor-kappaB (NF-kappaB) pathway, endothelial cells were treated with ox-LDL (100 microg/mL) for 2 h, and NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, intracellular ROS level, and NF-kappaB activity were measured. The results showed that reinioside C attenuated ox-LDL-induced NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, generation of ROS, and activation of NF-kappaB in endothelial cells in a dose-dependent manner; the two latter effects were inhibited by pyrollidine dithiocarbamate, the inhibitor of NF-kappaB. These findings suggest that reinioside C attenuates ox-LDL-induced expression of adhesion molecules (P-selectin and ICAM-1) and the adhesion of monocytes to endothelial cells by inhibiting NADPH oxidase/ROS/NF-kappaB pathway.

Moral issues have been included in the studies of consumer misbehavior research, but little is known about the joint moderating effect of moral intensity and moral judgment on the consumer’s use intention of pirated software. This study aims to understand the consumer’s use intention of pirated software in Taiwan based on the theory of planned behavior (TPB) proposed by Ajzen (Organizational Behavior and Human Decision Processes, 50, 179, 1991). In addition, moral intensity and moral judgment are adopted as a joint moderator to examine their combined influence on the proposed research framework. The results obtained from this Taiwan case reveal that the antecedent constructs proposed in the TPB model–an individual’s attitude and subjective norms toward using pirated software, and perceived behavioral control to use pirated software–indeed have positive impacts on the consumer’s use intention of pirated software. In addition, the joint moderating effect of moral intensity and moral judgment is manifested in the consumer’s use intention of pirated software. The results of this study not only could substantiate the results of consumer misbehavior research, but also could provide some managerial suggestions for Taiwanese government authorities concerned and the related software industries devoted to fighting pirated software.

To test whether treatment with fenofibrate decreases asymmetric dimethylarginine (ADMA) level in hypertriglyceridemic individuals.In the present study, 45 subjects with hypertriglyceridemia were recruited to receive treatment with fenofibrate (200 mg/d). Serum concentrations of ADMA, malondialdehyde (MDA), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) were measured. Endothelial function assessed by flow-mediated dilation (FMD) of the brachial artery was performed.Compared with control, serum levels of ADMA (0.47+/-0.05 micromol/L in control and 0.62+/-0.28 micromol/L in hypertriglyceridemic patients, P0.01), MDA and TNF-alpha were markedly elevated, and the level of NO was significantly reduced, concomitantly with impaired endothelium-dependent vasodilation in individuals with hypertriglyceridemia. 8-week treatment with fenofibrate significantly reduced the elevated levels of ADMA (0.53+/-0.12 micromol/L, P0.01), MDA and TNF-alpha, attenuated the decreased level of NO and improved endothelial function.These results suggest that the beneficial effect of fenofibrate on the endothelium in hypertriglyceridemic individuals may be related to reduction of ADMA level.

Previous investigations have demonstrated that endogenous inhibitors of nitric oxide synthase (NOS), such as asymmetric dimethylarginine (ADMA), contribute importantly to endothelial dysfunction, and that fenofibrate has a protective effect on the endothelium in rats treated with low-density lipoprotein (LDL) by reducing ADMA levels. In the present study, we explored further the possible mechanism underlying inhibition of ADMA generation by fenofibrate in cultured human umbilical vein endothelial cells (HUVECs). Endothelial injury was induced in cultured HUVECs by incubation with oxidative LDL (ox-LDL) and the levels of ADMA, lactate dehydrogenase (LDH), NO and tumour necrosis factor-alpha (TNF-alpha) in the conditioned medium were measured. Cell viability and the activity of dimethylarginine dimethylaminohydrolase (DDAH) and nuclear factor-kappaB (NF-kappaB) in the cultured HUVECs were also determined. Incubation of HUVECs with ox-LDL (100 microg/ml) for 24 h markedly elevated ADMA, LDH and TNF-alpha in the conditioned medium and significantly increased the activity of NF-kappaB, concomitantly with a significant decrease in the activity of DDAH and the content of NO. Pretreatment with fenofibrate (3, 10 or 30 microM) significantly inhibited the increases in ADMA, LDH and TNF-alpha, attenuated the decreased levels of NO and the decreased activity of DDAH and prevented the activation of NF-kappaB. Similar effects were observed in the presence of pyrrolidine dithiocarbamate (PDTC, 10 microM), an antagonist of NF-kappaB. The beneficial effects of fenofibrate on cultured endothelial cells were abolished by MK-886, a specific peroxisome proliferator-activated receptor-alpha (PPARalpha) antagonist. The present results suggest that fenofibrate inhibits ox-LDL-induced endothelial cell damage by decreasing ADMA and increasing DDAH activity, and the protective effects of fenofibrate on endothelial cells may be related to reduction of NF-kappaB activity by activation of the PPARalpha receptor.

Background Accumulation of advanced glycation end products (AGEs) in the vasculature triggers a series of morphological and functional changes contributing to endothelial hyperpermeability. The reorganisation and redistribution of the cytoskeleton regulated by profilin-1 mediates endothelial cell contraction, which results in vascular hyperpermeability. This study aimed to investigate the pivotal role of profilin-1 in the process of endothelial cell damage induced by AGEs. Methods Human umbilical vein endothelial cells (HUVECs) were incubated with AGEs. The mRNA and protein expression of profilin-1 was determined using real-time PCR and western blotting analyses. The levels of intercellular adhesion molecule-1 (ICAM-1), nitric oxide (NO) and reactive oxygen species (ROS), as well as the activities of nuclear factor-κB (NF-κB) and protein kinase C (PKC), were detected using the appropriate kits. The levels of asymmetric dimethylarginine (ADMA) were determined using HPLC. The distribution of the cytoskeleton was visualised using immunofluorescent staining. Results Compared with the control, incubation of endothelial cells with AGEs (200 μg/ml) for 4 or 24 h significantly up-regulated the mRNA and protein expression of profilin-1, markedly increased the levels of ICAM-1 and ADMA and decreased the production of NO (PP0.05). Conclusions These findings suggested that profilin-1 might act as an ultimate and common cellular effector in the process of metabolic memory (endothelial abnormalities) mediated by AGEs via the ROS/PKC or ROS/NF-қB signalling pathways.

Previous investigations have demonstrated that asymmetric dimethylarginine (ADMA) is an important factor contributing to endothelial dysfunction, and that fenofibrate has a protective effect on the endothelium in hyperlipidaemic patients. In the present study in rats treated with native low-density lipoprotein (nLDL), we addressed the question of whether the beneficial effect of fenofibrate on endothelial cells is related to reduction of the ADMA concentration. A single injection of nLDL (4 mg/kg, 48 h) markedly reduced endothelium-dependent relaxation in response to acetylcholine and the plasma level of nitrite/nitrate and increased the plasma concentrations of ADMA, malonyldialdehyde (MDA) and tumour necrosis factor-alpha (TNF-alpha). Treatment with fenofibrate (30 or 100 mg/kg) significantly reduced the inhibition of vasodilator responses to acetylcholine, decreased the elevated levels of ADMA, MDA and TNF-alpha, and enhanced the decreased level of nitrite/nitrate in the rats treated with LDL. These results suggest that the protective effect of fenofibrate on endothelial cells in rats treated with LDL may be related to the reduction of ADMA concentration.