9,437 research outputs found
Control of a lane-drop bottleneck through variable speed limits
In this study, we formulate the VSL control problem for the traffic system in
a zone upstream to a lane-drop bottleneck based on two traffic flow models: the
Lighthill-Whitham-Richards (LWR) model, which is an infinite-dimensional
partial differential equation, and the link queue model, which is a
finite-dimensional ordinary differential equation. In both models, the
discharging flow-rate is determined by a recently developed model of capacity
drop, and the upstream in-flux is regulated by the speed limit in the VSL zone.
Since the link queue model approximates the LWR model and is much simpler, we
first analyze the control problem and develop effective VSL strategies based on
the former. First for an open-loop control system with a constant speed limit,
we prove that a constant speed limit can introduce an uncongested equilibrium
state, in addition to a congested one with capacity drop, but the congested
equilibrium state is always exponentially stable. Then we apply a feedback
proportional-integral (PI) controller to form a closed-loop control system, in
which the congested equilibrium state and, therefore, capacity drop can be
removed by the I-controller. Both analytical and numerical results show that,
with appropriately chosen controller parameters, the closed-loop control system
is stable, effect, and robust. Finally, we show that the VSL strategies based
on I- and PI-controllers are also stable, effective, and robust for the LWR
model. Since the properties of the control system are transferable between the
two models, we establish a dual approach for studying the control problems of
nonlinear traffic flow systems. We also confirm that the VSL strategy is
effective only if capacity drop occurs. The obtained method and insights can be
useful for future studies on other traffic control methods and implementations
of VSL strategies.Comment: 31 pages, 14 figure
Determination of multifractal dimensions of complex networks by means of the sandbox algorithm
Complex networks have attracted much attention in diverse areas of science
and technology. Multifractal analysis (MFA) is a useful way to systematically
describe the spatial heterogeneity of both theoretical and experimental fractal
patterns. In this paper, we employ the sandbox (SB) algorithm proposed by
T\'{e}l et al. (Physica A, 159 (1989) 155-166), for MFA of complex networks.
First we compare the SB algorithm with two existing algorithms of MFA for
complex networks: the compact-box-burning (CBB) algorithm proposed by Furuya
and Yakubo (Phys. Rev. E, 84 (2011) 036118), and the improved box-counting (BC)
algorithm proposed by Li et al. (J. Stat. Mech.: Theor. Exp., 2014 (2014)
P02020) by calculating the mass exponents tau(q) of some deterministic model
networks. We make a detailed comparison between the numerical and theoretical
results of these model networks. The comparison results show that the SB
algorithm is the most effective and feasible algorithm to calculate the mass
exponents tau(q) and to explore the multifractal behavior of complex networks.
Then we apply the SB algorithm to study the multifractal property of some
classic model networks, such as scale-free networks, small-world networks, and
random networks. Our results show that multifractality exists in scale-free
networks, that of small-world networks is not obvious, and it almost does not
exist in random networks.Comment: 17 pages, 2 table, 10 figure
Multifractal analysis of weighted networks by a modified sandbox algorithm
Complex networks have attracted growing attention in many fields. As a
generalization of fractal analysis, multifractal analysis (MFA) is a useful way
to systematically describe the spatial heterogeneity of both theoretical and
experimental fractal patterns. Some algorithms for MFA of unweighted complex
networks have been proposed in the past a few years, including the sandbox (SB)
algorithm recently employed by our group. In this paper, a modified SB
algorithm (we call it SBw algorithm) is proposed for MFA of weighted
networks.First, we use the SBw algorithm to study the multifractal property of
two families of weighted fractal networks (WFNs): "Sierpinski" WFNs and "Cantor
dust" WFNs. We also discuss how the fractal dimension and generalized fractal
dimensions change with the edge-weights of the WFN. From the comparison between
the theoretical and numerical fractal dimensions of these networks, we can find
that the proposed SBw algorithm is efficient and feasible for MFA of weighted
networks. Then, we apply the SBw algorithm to study multifractal properties of
some real weighted networks ---collaboration networks. It is found that the
multifractality exists in these weighted networks, and is affected by their
edge-weights.Comment: 15 pages, 6 figures. Accepted for publication by Scientific Report
Estradiol regulates miR-135b and mismatch repair gene expressions via estrogen receptor-β in colorectal cells.
Estrogen has anti-colorectal cancer effects which are thought to be mediated by mismatch repair gene (MMR) activity. Estrogen receptor (ER) expression is associated with microRNA (miRNA) expression in ER-positive tumors. However, studies of direct link between estrogen (especially estradiol E2), miRNA expression, and MMR in colorectal cancer (CRC) have not been done. In this study, we first evaluated the effects of estradiol (E2) and its antagonist ICI182,780 on the expression of miRNAs (miR-31, miR-155 and miR-135b) using COLO205, SW480 and MCF-7 cell lines, followed by examining the association of tissue miRNA expression and serum E2 levels using samples collected from 18 colorectal cancer patients. E2 inhibited the expressions of miRNAs in COLO205 cells, which could be reversed by E2 antagonist ICI 182.780. The expression of miR-135b was inversely correlated with serum E2 level and ER-β mRNA expression in CRC patients' cancer tissues. There were significant correlations between serum E2 level and expression of ER-β, miR-135b, and MMR in colon cancer tissue. This study suggests that the effects of estrogen on MMR function may be related to regulating miRNA expression via ER-β, which may be the basis for the anti-cancer effect in colorectal cells
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