2,364 research outputs found
Radio Resource Allocation for Device-to-Device Underlay Communication Using Hypergraph Theory
Device-to-Device (D2D) communication has been recognized as a promising
technique to offload the traffic for the evolved Node B (eNB). However, the D2D
transmission as an underlay causes severe interference to both the cellular and
other D2D links, which imposes a great technical challenge to radio resource
allocation. Conventional graph based resource allocation methods typically
consider the interference between two user equipments (UEs), but they cannot
model the interference from multiple UEs to completely characterize the
interference. In this paper, we study channel allocation using hypergraph
theory to coordinate the interference between D2D pairs and cellular UEs, where
an arbitrary number of D2D pairs are allowed to share the uplink channels with
the cellular UEs. Hypergraph coloring is used to model the cumulative
interference from multiple D2D pairs, and thus, eliminate the mutual
interference. Simulation results show that the system capacity is significantly
improved using the proposed hypergraph method in comparison to the conventional
graph based one.Comment: 27 pages,10 figure
Porcellio scaber algorithm (PSA) for solving constrained optimization problems
In this paper, we extend a bio-inspired algorithm called the porcellio scaber
algorithm (PSA) to solve constrained optimization problems, including a
constrained mixed discrete-continuous nonlinear optimization problem. Our
extensive experiment results based on benchmark optimization problems show that
the PSA has a better performance than many existing methods or algorithms. The
results indicate that the PSA is a promising algorithm for constrained
optimization.Comment: 6 pages, 1 figur
Role of apolipoprotein E isoforms and cytokines in immune responses and inflammation of the mouse peripheral nervous system
Experimental autoimmune neuritis (EAN) as an animal model for Guillain-Barré syndrome
(GBS) in humans is an immune-mediated disorder affecting the peripheral nervous system
(PNS). Apolipoprotein E (apoE) is a glycosylated protein characterized by its wide tissue
distribution and multiple biological functions. ApoE can suppress proinflammatory signalings,
and vice versa, indicating an intricate apoE-mediated feedback regulation of inflammatory and
immune responses. Immune cells together with cytokines produced by various cells contribute to
the inflammatory process of EAN by acting as mediators or effectors.
In Paper I, the effects of apoE isoforms on the functions of immune cells were investigated.
Clinical signs of EAN were most severe in wild type (WT) C57BL/6 mice and apoE4 transgenic
(Tg) mice, followed by apoE2 Tg mice and apoE3 Tg mice (WT ≈ E4 > E2 > E3). Proliferation
tests of purified T cells from naive mice stimulated with phytohemagglutinin or interleukin (IL)-
12 showed isoform-specific differences (WT ≈ E4 > E3 ≈ E2). Macrophages from both naïve
and EAN mice produced nitric oxide (NO) upon inflammatory stimulation in an isoformdependent manner (WT ≈ E4 > E2 > E3). During the recovery stage of disease, the highest
expression of CD178 (FasL) on Schwann cells (SCs) was found in apoE3 Tg mice. In Paper II,
the effects of different isoforms of apoE on SCs in response to inflammatory stimulation
(lipopolysaccharide plus interferon (IFN)-γ) were studied. Upon stimulation, a change in the
morphology of cultured SCs was observed. Pronounced production of IL-6 and IL-10 within SCs,
and increased levels of IL-6 and NO in culture supernatants were found in an isoform-dependent
manner (apoE3 > apoE2 ≈ apoE4). Further results indicated that both nuclear factor kappa B
(NFκB) and Akt signaling pathways were involved in the process by the same isoformdependent pattern. In Paper III, the role of IFN-γ, a signature T helper (Th)1 cytokine, in the
pathogenesis of EAN was investigated. The clinical signs of EAN in IFN-γ knockout (KO) mice
were evidently aggravated. At the peak of EAN, the proportion of IL-17A expressing cells in
cauda equina (CE) infiltrating cells, and the serum levels of IL-17A were elevated in IFN-γ KO
mice. The proportions of MHC II, macrosialin, and IL-12/IL-23p40 expressing cells, relative to
total CE infiltrating cells were correspondingly higher in IFN-γ KO than WT mice with EAN. In
Paper IV, the role of tumor necrosis factor alpha (TNF-α), another Th1 cytokine, in the
pathogenesis of EAN was studied. TNF-α deficiency significantly attenuated EAN. Furthermore,
TNF-α deficiency induced an antiinflammatory phenotype of macrophages (M2) characterized
by reduced production of IL-12 and NO, and enhanced production of IL-10. Moreover, TNF
receptor (TNFR)1 monoclonal antibodies markedly suppressed the severity of EAN when they
were administered from the beginning of EAN induction.
In summary, our data support an isoform-dependent effect of apoE on EAN. This might be due
to the isoform-specific effects of apoE on functions of T cells, macrophages and SCs, which
contribute to the distinct clinical courses of EAN. SCs from apoE2 and apoE4 Tg mice bear
some dysfunction in producing cytokines (IL-6 and IL-10) and NO as compared with their
apoE3 counterparts, probably resulting from their insufficiency to suppress the activation of
NFκB and Akt pathways. IFN-γ deficiency exacerbates EAN via upregulating Th17 cells despite
a mitigated systemic Th1 immune response. TNF-α exacerbates EAN via TNFR1 by inducing
the proinflammatory phenotype of macrophage (classically activated macrophage, M1)
Vertex-Coloring 2-Edge-Weighting of Graphs
A -{\it edge-weighting} of a graph is an assignment of an integer
weight, , to each edge . An edge weighting naturally
induces a vertex coloring by defining for every
. A -edge-weighting of a graph is \emph{vertex-coloring} if
the induced coloring is proper, i.e., for any edge .
Given a graph and a vertex coloring , does there exist an
edge-weighting such that the induced vertex coloring is ? We investigate
this problem by considering edge-weightings defined on an abelian group.
It was proved that every 3-colorable graph admits a vertex-coloring
-edge-weighting \cite{KLT}. Does every 2-colorable graph (i.e., bipartite
graphs) admit a vertex-coloring 2-edge-weighting? We obtain several simple
sufficient conditions for graphs to be vertex-coloring 2-edge-weighting. In
particular, we show that 3-connected bipartite graphs admit vertex-coloring
2-edge-weighting
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