Life Cycle Costs Analysis of Reclaimed Asphalt Pavement (RAP) Under Future Climate

Reclaimed asphalt pavement (RAP) has received wide application in asphalt pavement construction and maintenance and it has shown cost-effectiveness over virgin hot mix asphalt (HMA). HMA with a high content of reclaimed asphalt (RA) (e.g., 40%) is sometimes used in practice, however, it may have significant adverse effects on the life cycle performance and related costs. In particular, challenges may arise as the life cycle performance of RAP is also affected by local climatic conditions. Thus, it is important to investigate whether it is still economic to use RAP under future local climate, with consideration of life cycle performance. A case study was conducted for various road structures on Interstate 95 (I-95) in New Hampshire (NH), USA for the investigation. The case study utilized dynamic modulus testing results for local virgin HMA and HMA with 40% RA (as major material alternatives) to predict life cycle performance of the selected pavement structures, considering downscaled future climates. Then, a life cycle cost analysis (LCCA) was considered to estimate and compare the life cycle cash flow of the investigated road structures. Responsive maintenance (overlay) and effectiveness were also considered in this study. It was found that using 40% RA in HMA can reduce agency costs by up to approximately 18% under the 2020–2040 predicted climate and NH should consider this practice under predicted future climate to reduce agency costs

Mitochondrial Superoxide Contributes to Blood Flow and Axonal Transport Deficits in the Tg2576 Mouse Model of Alzheimer's Disease

Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive decline in cognitive functions and the deposition of aggregated amyloid beta (Abeta) into senile plaques and the protein tau into tangles. In addition, a general state of oxidation has long been known to be a major hallmark of the disease. What is not known however, are the mechanisms by which oxidative stress contributes to the pathology of AD.In the current study, we used a mouse model of AD and genetically boosted its ability to quench free radicals of specific mitochondrial origin. We found that such manipulation conferred to the AD mice protection against vascular as well as neuronal deficits that typically affect them. We also found that the vascular deficits are improved via antioxidant modulation of the endothelial nitric oxide synthase, an enzyme primarily responsible for the production of nitric oxide, while neuronal deficits are improved via modulation of the phosphorylation status of the protein tau, which is a neuronal cytoskeletal stabilizer.These findings directly link free radicals of specific mitochondrial origin to AD-associated vascular and neuronal pathology

How to Motivate Employees’ Environmental Citizenship Behavior through Perceived Interpersonal Circle Power? A New Perspective from Chinese Circle Culture

Employees’ spontaneous environmental citizenship behavior (ECB) is a key factor in facilitating the low-carbon transition of enterprises. However, little research has focused on the impact of interpersonal interactions on ECB. To explore how ECB is affected by special interpersonal circles in Chinese organizations, we propose a new concept: perceived interpersonal circle power (PICP). From the two dimensions of PICP, leader-oriented perceived interpersonal circle power (PICP-L) and colleague-oriented perceived interpersonal circle power (PICP-C), we establish a mechanism model to explore the effect of PICP on ECB. A structural equation model was used to test our hypotheses through 332 questionnaires, and the results show that PICP-L and PICP-C differ significantly in the directions and strengths of their effects on ECB. PICP-C has a direct positive driving effect on environmental engagement behavior (EEB) and environmental helping behavior (EHB). High PICP-C can also encourage EEB via affective organizational commitment (AOC). Conversely, PICP-L has no significant effect on EEB. More unexpectedly, PICP-L has a significant negative influence on EHB. This study provides a new direction for future theoretical research on ECB, as well as a new opportunity for policy-making and enterprise management practices to promote employees’ ECB

Analysis of the Cause of Household Carbon Lock-In for Chinese Urban Households

Household energy conservation is an important contributor to achieve the carbon emission reduction target. However, the actual energy-saving effect of Chinese households is under expectation. One reason for this is because household energy consumption is locked in at a certain level, which has become an obstacle to household carbon emission reduction. In order to reduce this obstacle, this study explored the cause of household carbon lock-in based on grounded theory, targeting newly furnished households. A theoretical model was developed to reveal the formation mechanism of carbon lock-in effect in the purchasing process of household energy-using appliances. NVivo 12 software was used to analyze the decoration diaries of 616 sample households, and the results showed that (1) the direct antecedent of the household carbon lock-in effect was the lock-in of purchasing behavior, and the household carbon lock-in effect was mainly exhibited in the consumption path dependence (of energy-using appliances) and the solidification of energy structure; (2) the willingness to purchase household appliances was the direct antecedent of purchasing behavioral lock-in, and the cost had a moderating effect on the transformation from purchase willingness to behavioral lock-in; and (3) in the process of purchasing household appliances, reference groups, value perception, and ecological awareness can promote purchasing behavioral lock-in by affecting willingness of purchase. Suggestions to promote unlocking of household carbon were also proposed

Ampelopsin Improves Insulin Resistance by Activating PPARγ and Subsequently Up-Regulating FGF21-AMPK Signaling Pathway

<div><p>Ampelopsin (APL), a major bioactive constituent of <i>Ampelopsis grossedentata</i>, exerts a number of biological effects. Here, we explored the anti-diabetic activity of APL and elucidate the underlying mechanism of this action. In palmitate-induced insulin resistance of L6 myotubes, APL treatment markedly up- regulated phosphorylated insulin receptor substrate-1 and protein kinase B, along with a corresponding increase of glucose uptake capacity. APL treatment also increased expressions of fibroblast growth factor (FGF21) and phosphorylated adenosine 5’-monophosphate -activated protein kinase (p-AMPK), however inhibiting AMPK by Compound C or <i>AMPK</i> siRNA, or blockage of <i>FGF21 by FGF21</i> siRNA, obviously weakened APL -induced increases of FGF21 and p-AMPK as well as glucose uptake capacity in palmitate -pretreated L6 myotubes. Furthermore, APL could activate PPAR γ resulting in increases of glucose uptake capacity and expressions of FGF21 and p-AMPK in palmitate -pretreated L6 myotubes, whereas all those effects were obviously abolished by addition of GW9662, a specific inhibitor of peroxisome proliferator- activated receptor –γ (PPARγ), and <i>PPARγsiRNA</i>. Using molecular modeling and the luciferase reporter assays, we observed that APL could dock with the catalytic domain of PPARγ and dose-dependently up-regulate PPARγ activity. In summary, APL maybe a potential agonist of PPARγ and promotes insulin sensitization by activating PPARγ and subsequently regulating FGF21- AMPK signaling pathway. These results provide new insights into the protective health effects of APL, especially for the treatment of Type 2 diabetes mellitus.</p></div

APL improved palmitate -induced insulin resistance through activating AMPK in skeletal muscle myotubes.

<p><b>(A)</b>. Differentiated L6 cells were untreated or pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). Western blots detected p-AMPK and AMPK <b>(B)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 1, 5 or 10 μM APL for another 24 h in the presence of insulin (100 nM). Western blots detected p-AMPK and AMPK. <b>(C)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with (10 μM) of APL for 6, 12 or 24 h in the presence of insulin (100 nM). Western blots detected p-AMPK and AMPK. <b>(D)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then with CC (10 μM) for 1 h or transfection with AMPK siRNA for 24 h,respectively, following by treated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). Total L6 cell lysates were used for western blots. <b>(E)</b> Differentiated L6 cells were treated as described in (D). Cells were collected and 2-NBDG glucose uptake was assessed. Values are means ± SEM. n = 3, ^a<i>p</i> < 0.05 palmitate -treated group; ^b<i>p</i> < 0.05 versus APL and palmitate co-treated group. All results are representative western blots of three independent experiments with similar results.</p

PPARγ activation was involved in APL-mediated FGF21 up-regulation in skeletal muscle myotubes.

<p><b>(A)</b> Differentiated L6 cells were untreated or pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). PPARγ was detected by western blot. <b>(B)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, and then incubated with 1, 5 or 10 μM APL for 24 h. PPARγ was detected by western blot. <b>(C)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, and then incubated with (10 μM) APL for 6, 12 or 24 h. PPARγ was detected by western blot. <b>(D)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then cells were treated with GW9662 (10 μM) for 1 h, or following by treated with 10 μM APL or Rosiglitazone (Ros) (10 μM) for 24 h in the presence of insulin (100 nM). Total L6 cell lysates were used for western blots. <b>(E)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then transfected with <i>PPARγ</i> siRNA for 24h, following by treated with 10 μM APL or Rosiglitazone (Ros) (10 μM) for 24 h in the presence of insulin (100 nM). Total L6 cell lysates were used for western blots. <b>(F)</b> Molecular modeling of the interaction between APL and PPARγ. A close-up view of the consensus orientation for APL is shown. The PPARγ protein is depicted as a ribbon representation and colored by secondary structures (i.e., helix, strand, and loop) (left panel); the hydrogen bonds between APL and PPARγ(distance<3.2 Å) are depicted as red dotted lines that include the names of the residues and distances (right panel). <b>(G)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then cells were treated with GW9662 for 1 h or <i>PPARγ</i> siRNA for 24 h before addition of APL (10 μM) or Ros(10 μM) in the presence or absence of insulin (100 nM). Cells were collected and 2-NBDG glucose uptake was assessed. Values are means ± SEM. n = 3, ^a<i>p</i> < 0.05 versus palmitate -treated group; ^b<i>p</i> < 0.05 versus APL and palmitate co-treated group; ^c<i>p</i> < 0.05 versus Ros and palmitate co-treated group. All results are representative western blots of three independent experiments with similar results. (H)Activation effect of APL and rosiglitazone (Ros) on hPPARγ. The activity of the vehicle control was set at 1 and the relative luciferase activities are presented as fold induction relative to the vehicle control. ^a<i>p</i> < 0.05 versus control group. n = 3. Mean±SD.</p

AMPK activation depended on APL-induced up-regulation of FGF21 expression in skeletal muscle myotubes.

<p><b>(A)</b> Differentiated L6 cells were untreated or pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). FGF21 expression was detected by western blot. <b>(B)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, and then incubated with 1, 5 or 10 μM APL for 24 h. FGF21 expression was detected by western blot. <b>(C)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with (10 μM) of APL for 6, 12 or 24 h. FGF21 was detected by western blot. <b>(D)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then transfected with <i>FGF21</i> siRNA before addition of APL (10 μM) for 24 h in the presence of insulin (100 nM). Total L6 cell lysates were used for western blots. <b>(E)</b> Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then transfection with FGF21 siRNA for 24 h, following by treated with 10 μM APL, FGF21 protein (4.0μg/mL) or APL and FGF21 protein for 24 h, respectively,in the presence or absence of insulin (100 nM). Cells were collected and 2-NBDG glucose uptake was assessed. Values are means ± SEM. n = 3, ^a<i>p</i> < 0.05 versus palmitate -treated group; ^<i>b</i><i>p</i> < 0.05 versus APL and palmitate co-treated group. ^c<i>p</i> < 0.05 versus APL, <i>FGF21</i> siRNA and palmitate co-treated group. All results are representative western blots of three independent experiments with similar results.</p