Influential factors of environmental behavior to reduce air pollution: integrating theories of planned behavior and psychological distance

Exploring the incentive mechanism of public participation is the key to the implementation of sustainable policies in China. This study related the constructs of psychological distance (PD), the theory of planned behavior (TPB) and willingness to pay (WTP) to examine the influential factors of environmental behaviors to prevent air pollution. The contingent valuation method was applied to demonstrate pro-environmental endeavors by measuring WTP and the structural equation model was used to clarify the effects between PD, TPB and WTP. The results showed that different dimensions of PD from air pollution have overlapping influences. Participants judged the air pollution as psychologically closer tend to have positive attitudes and stronger subjective norms, and the reduced PD can translate into increased WTP. The PD-TPB-WTP model correctly predicts up to 17.6% of WTP and 82.6% of behavioral intention. Environmental policymakers are suggested to draft policies according to individuals’ internal thinking.</p

Chemical composition and biological activities of the essential oil from <i>Rubus pungens</i> var. <i>oldhamii</i>

<p>This paper presents a study on chemical composition, antimicrobial, antioxidant and tyrosinase inhibitory properties of the essential oil from leaves of <i>Rubus pungens</i> var. <i>oldhamii</i> (REO). The major component of the REO is sesquiterpenes (36.04%), which consists of 1,5-Cyclooctadiene,3-(1-me thylallyl)-(8CI)(17.66%), 5,6-Diethenyl-1-methylcyclohexene (12%), (+) – γ-Elemene (10.48%) and β-Caryophyllene (8.39%).The REO is shown to be moderately active against <i>Staphylococcus</i> <i>aureus,</i> <i>Aspergillus</i> <i>niger</i> and <i>Penicillium</i> <i>glaucum</i>, and has weak antioxidant activity in 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. Furthermore, tyrosinase inhibition was investigated against monophenolase (L-tyrosine). IC₅₀ values of REO and arbutin were found 0.923 and 0.657 mg/mL, respectively. The REO exerted potential antityrosinase activity. Our test results indicated that the REO was rich in sesquiterpenes, and also exhibited good antityrosinase activity, and moderate antimicrobial activity against pathogenic micro-organisms. The REO can be used as a natural source of promising antimicrobial and tyrosinase inhibiting agent.</p

How does air pollution risk perception affect residents’ subjective well-being? A structural equation model approach

Air pollution has caused many risks to people, but little research has been done on the effect of residents’ air pollution risk perception on their subjective well-being. In order to reveal their relationship, this paper divides air pollution risk perception into four dimensions: risk controllability, risk trust, risk acceptability and risk effect, and explores the effects of different dimensions of air pollution risk perception on subjective well-being based on the structural equation model. The results show that risk controllability, risk trust and risk acceptability can improve well-being, while risk effect can reduce well-being, and air quality satisfaction plays a mediating role. There are also internal influencing mechanisms among different air pollution risk perceptions. Particularly, in areas with poor air quality, risk controllability had a negative association with air quality satisfaction, and higher risk effect corresponded to a higher degree of risk controllability. This paper provides some suggestions for environmental management from the perspective of risk perception.</p

Inhibition of Akt enhances sorafenib-induced growth inhibition and apoptosis.

<p>A-B, HepG2 and Huh7 cells were exposed to 100 nM bufalin and/or 5 μM of sorafenib in the presence or absence of perifosine (10 μM) for 48 h. (A) Cell viability (%) was then compared with the corresponding untreated cells. (B) The percentages of apoptotic cells (%) were measured by flow cytometry. Untransfected cells served as controls. C-D, HepG2 and Huh7 cells were transfected with control or Akt siRNA for 24 h and then incubated with 100 nM bufalin, 5 μM sorafenib, or a combination of the two drugs for 24 h. (C) Cell viability (%) was compared with control siRNA-transfected cells. (D) The percentages of apoptotic cells (%) were measured by flow cytometry. Untransfected cells served as controls. The data represent three independent experiments. “**” represents P<0.001.</p

Bufalin suppresses sorafenib-induced Akt activation to reverse resistance to sorafenib in HCC cells.

<p>A-B, Huh7 cells were exposed to different concentrations of bufalin (A) or to 100 nM bufalin and/or 5 μM sorafenib (B) for 48 h. Untreated cells served as controls. Cell lysates were immunoblotted, and the density of each band was measured. Band densities were normalized to β-actin. The relative band density from untreated cells was defined as 1. (C) The Huh7 cells from (B) were immunostained with anti-p-Akt Ab (red) and DAPI (cellular nuclei, blue) and viewed with an inverted fluorescence microscope. The data represent three independent experiments. “*” (P<0.05) and “**” (P<0.001) vs. untreated control; “‡” (P<0.001) vs. sorafenib alone.</p

Bufalin-induced Akt inactivation is IRE1 dependent.

<p>(A) Huh7 cells were exposed to 100 nM bufalin for 12, 24, or 48 h. Untreated cells served as controls. Cell lysates were immunoblotted, and the density of each band was measured. Band densities were normalized to β-actin. (B) Huh7 cells were transfected with control, eIF2α, CHOP, or IRE1 siRNA for 24 h and then incubated with 100 nM bufalin for 24 h. Cell lysates were immunoblotted, and the density of each band was measured. Band densities were normalized to β-actin. The relative band density from control-siRNA transfected cells was defined as 1. (C) Huh7 cells were transfected with control or Akt siRNA for 24 h and then incubated with 100 nM bufalin for 24 h. Cell lysates were immunoblotted, and the density of each band was measured. Band densities were normalized to β-actin. The relative band density from control-siRNA transfected cells was defined as 1. (D) Huh7 cells were incubated with 100 nM bufalin and/or 5 μM sorafenib for 48 h. The cells were immunostained with Abs against IRE1 (red) and p-Akt (green) as well as with DAPI (cellular nuclei, blue). The data represent three independent experiments. N.S., not significant. “*” (P<0.05) and “**” (P<0.001) vs. untreated control; “##” represents P<0.001.</p

Bufalin synergizes with sorafenib to induce apoptosis in HCC cells.

<p>HepG2 and Huh7 cells were incubated with 100 nM bufalin and/or 5 μM sorafenib for 48 h. (A) The cells were stained with Annexin V/PI and subjected to flow cytometry to measure the apoptosis rate (%). (B) Representative images were taken of Huh7 cells stained with Annexin V/PI and viewed with a laser-scanning confocal microscope. (C) The activities of caspase-3 and caspase-9 were measured. The data represent three independent experiments. Untreated cells served as controls. “*” (P<0.05) and “**” (P<0.001) vs. untreated control; “‡” (P<0.001) vs. sorafenib alone; “#” (P<0.05) and “##” (P<0.001) vs. bufalin alone.</p

Bufalin reverses acquired resistance to sorafenib by downregulating p-Akt via IRE1 activation.

<p>(A) Huh7 and Huh7-Sora cells were cultured in complete medium, and the viability was examined after 24, 48, and 72 h in culture. (B) The above cells were exposed to increasing concentrations of sorafenib for 48 h. Untreated cells served as controls. Cell viability (%) was compared to the corresponding untreated cells. (C) The above cells were exposed to increasing concentrations of bufalin for 48 h. Untreated cells served as controls. Cell viability (%) was compared with the corresponding untreated cells. The black line indicates the IC50. (D) The lysates of cells from (A) were subjected to immunoblotting. Band densities were normalized to β-actin. The relative band density from Huh7 cells was defined as 1. (E) Huh7-Sora cells were transfected with control or IRE1 siRNA for 24 h and then incubated with 100 nM bufalin for 24 h. Cell lysates were immunoblotted, and the density of each band was measured. Band densities were normalized to β-actin. The relative band density from control cells was defined as 1. The data represent three independent experiments. N.S., not significant. “*” represents P<0.05, “**” represents P<0.001.</p

The siRNAs used in this study and their targeted genes.

<p>Abbreviations: IRE1, inositol-requiring enzyme 1; eIF2, eukaryotic initiation factor 2; CHOP, C/EBP-homologous protein.</p><p>The siRNAs used in this study and their targeted genes.</p

Bufalin synergizes with sorafenib to inhibit HCC cell growth.

<p>(A) HepG2 and Huh7 cells were exposed to different concentrations of bufalin and/or sorafenib for 48 h. (B) The above cells were incubated with 100 nM bufalin and/or 5 μM sorafenib for different periods. Cell viability (%) was then compared with the corresponding untreated cells. The data represent three independent experiments. “**” (P<0.001) vs. bufalin alone. “†” (P<0.05) and “‡” (P<0.001) vs. sorafenib alone.</p