Engineering topics
Liu, Ju
Publications and source records attributed to Liu, Ju.
Multiobjective Model of Time-of-Use and Stepwise Power Tariff for Residential Consumers in Regulated Power Markets
Here, time-of-use (TOU) rates and stepwise power tariff (SPT) are important economic levers to motivate residents to shift their electricity usage in response to electricity price. In this paper, a new multiobjective optimal tariff-making model of time-of-use and stepwise power tariff (TOUSPT) is proposed, which combines the complementary characteristics of two power tariffs, for residential energy conservation and peak load shaving. In the proposed approach, the residential demand response with price elasticity in regulated power market is considered to determine the optimum peak-valley TOU tariffs for each stepwise electricity partition. Furthermore, a practical case study is implemented to test the effectiveness of the proposed TOUSPT, and the results demonstrate that TOUSPT can achieve efficient end-use energy saving and also shift load from peak to off-peak periods.
Trichostatin A suppresses lung adenocarcinoma development in Grg1 overexpressing transgenic mice
Trichostatin A (TSA) is a histone deacetylase inhibitor and a potential therapeutic for various malignancies. The in vivo effect of TSA, however, has not been investigated in a transgenic lung cancer model. Previously, we generated transgenic mice with overexpression of Groucho-related-gene 1 (Grg1) and these mice all developed mucinous lung adenocarcinoma. Grg1 is a transcriptional co-repressor protein, the function of which is thought to depend on HDAC activity. However, functions outside the nucleus have also been proposed. We tested the supposition that Grg1-induced tumorigenesis is HDAC-dependent by assaying the therapeutic effect of TSA in the Grg1 transgenic mouse model. We found that TSA significantly inhibited lung tumorigenesis in Grg1 transgenic mice (p < 0.01). TSA did not affect overall Grg1 protein levels, but instead reduced ErbB1 and ErbB2 expression, which are upregulated by Grg1 in the absence of TSA. We confirmed this effect in A549 cells. Furthermore, lapatinib, an inhibitor of both ErbB1 and ErbB2, effectively masked the effect of TSA on the inhibition of A549 cell proliferation and migration, suggesting TSA does work, at least in part, by downregulating ErbB receptors. We additionally found that TSA reduced the expression of VEGF and VEGFR2, but not basic FGF and FGFR1. Our findings indicate that TSA effectively inhibits Grg1-induced lung tumorigenesis through the down-regulation of ErbB1 and ErbB2, as well as reduced VEGF signaling. This suggests TSA and other HDAC inhibitors could have therapeutic value in the treatment of lung cancers with Grg1 overexpression. - Highlights: • TSA suppresses lung tumorigenesis in Grg1 overexpressing transgenic mice. • TSA does not affect overall Grg1 protein levels in the mice and in A549 cells. • TSA reduces ErbB1 and ErbB2 expression in the mice and in A549 cells. • Lapatinib masks TSA-induced inhibition of A549 cell proliferation and migration. • TSA inhibits VEGF signaling, but not basic FGF signaling.
Cadmium induces vascular permeability via activation of the p38 MAPK pathway
Highlights: • Low-dose cadmium (Cd) induces vascular hyper-permeability. • p38 MAPK mediates Cd-induced disruption of endothelial cell barrier function. • SB203850 inhibits Cd-induced membrane dissociation of VE-cadherin and β-catenin. • SB203850 reduces Cd-induced expression and secretion of TNF-α. - Abstract: The vasculature of various organs is a targeted by the environmental toxin, cadmium (Cd). However, mechanisms leading to pathological conditions are poorly understood. In the present study, we examined the effect of cadmium chloride (CdCl{sub 2}) on human umbilical vein endothelial cells (HUVECs). At 4 μM, CdCl{sub 2} induced a hyper-permeability defect in HUVECs, but not the inhibition of cell growth up to 24 h. This effect of CdCl{sub 2} was dependent on the activation of the p38 mitogen-activated protein kinase (MAPK) pathway. The p38 MAPK inhibitor SB203850 suppressed the CdCl{sub 2}-induced alteration in trans-endothelial electrical resistance in HUVEC monolayers, a model measurement of vascular endothelial barrier integrity. SB203850 also inhibited the Cd-induced membrane dissociation of vascular endothelial (VE) cadherin and β-catenin, the important components of the adherens junctional complex. In addition, SB203850 reduces the Cd-induced expression and secretion of tumor necrosis factor α (TNF-α). Taken together, our findings suggest that Cd induces vascular hyper-permeability and disruption of endothelial barrier integrity through stimulation of p38 MAPK signaling.
Functional entropy variables: A new methodology for deriving thermodynamically consistent algorithms for complex fluids, with particular reference to the isothermal Navier–Stokes–Korteweg equations
We propose a new methodology for the numerical solution of the isothermal Navier–Stokes–Korteweg equations. Our methodology is based on a semi-discrete Galerkin method invoking functional entropy variables, a generalization of classical entropy variables, and a new time integration scheme. We show that the resulting fully discrete scheme is unconditionally stable-in-energy, second-order time-accurate, and mass-conservative. We utilize isogeometric analysis for spatial discretization and verify the aforementioned properties by adopting the method of manufactured solutions and comparing coarse mesh solutions with overkill solutions. Various problems are simulated to show the capability of the method. Our methodology provides a means of constructing unconditionally stable numerical schemes for nonlinear non-convex hyperbolic systems of conservation laws.