2,380 research outputs found
The Firefighter Problem: A Structural Analysis
We consider the complexity of the firefighter problem where b>=1 firefighters
are available at each time step. This problem is proved NP-complete even on
trees of degree at most three and budget one (Finbow et al.,2007) and on trees
of bounded degree b+3 for any fixed budget b>=2 (Bazgan et al.,2012). In this
paper, we provide further insight into the complexity landscape of the problem
by showing that the pathwidth and the maximum degree of the input graph govern
its complexity. More precisely, we first prove that the problem is NP-complete
even on trees of pathwidth at most three for any fixed budget b>=1. We then
show that the problem turns out to be fixed parameter-tractable with respect to
the combined parameter "pathwidth" and "maximum degree" of the input graph
Surfactant protein D modulates HIV infection of both T-cells and dendritic cells
Surfactant Protein D (SP-D) is an oligomerized C-type lectin molecule with immunomodulatory properties and involvement in lung surfactant homeostasis in the respiratory tract. SP-D binds to the enveloped viruses, influenza A virus and respiratory syncytial virus and inhibits their replication in vitro and in vivo. SP-D has been shown to bind to HIV via the HIV envelope protein gp120 and inhibit infectivity in vitro. Here we show that SP-D binds to different strains of HIV (BaL and IIIB) and the binding occurs at both pH 7.4 and 5.0 resembling physiological relevant pH values found in the body and the female urogenital tract, respectively. The binding of SP-D to HIV particles and gp120 was inhibited by the presence of several hexoses with mannose found to be the strongest inhibitor. Competition studies showed that soluble CD4 and CVN did not interfere with the interaction between SP-D and gp120. However, soluble recombinant DC-SIGN was shown to inhibit the binding between SP-D and gp120. SP-D agglutinated HIV and gp120 in a calcium dependent manner. SP-D inhibited the infectivity of HIV strains at both pH values of 7.4 and 5.0 in a concentration dependent manner. The inhibition of the infectivity was abolished by the presence of mannose. SP-D enhanced the binding of HIV to immature monocyte derived dendritic cells (iMDDCs) and was also found to enhance HIV capture and transfer to the T-cell like line PM1. These results suggest that SP-D can bind to and inhibit direct infection of T-cells by HIV but also enhance the transfer of infectious HIV particles from DCs to T-cells in vivo
Systems analysis of primary Sjögren's syndrome pathogenesis in salivary glands identifies shared pathways in human and a mouse model
Introduction: Primary Sjogren's syndrome (pSS) is a chronic autoimmune disease with complex etiopathogenesis. Despite extensive studies to understand the disease process utilizing human and mouse models, the intersection between these species remains elusive. To address this gap, we utilized a novel systems biology approach to identify disease-related gene modules and signaling pathways that overlap between humans and mice. Methods: Parotid gland tissues were harvested from 24 pSS and 16 non-pSS sicca patients and 25 controls. For mouse studies, salivary glands were harvested from C57BL/6.NOD-Aec1Aec2 mice at various times during development of pSS-like disease. RNA was analyzed with Affymetrix HG U133+2.0 arrays for human samples and with MOE430+2.0 arrays for mouse samples. The images were processed with Affymetrix software. Weighted-gene co-expression network analysis was used to identify disease-related and functional pathways. Results: Nineteen co-expression modules were identified in human parotid tissue, of which four were significantly upregulated and three were downregulated in pSS patients compared with non-pSS sicca patients and controls. Notably, one of the human disease-related modules was highly preserved in the mouse model, and was enriched with genes involved in immune and inflammatory responses. Further comparison between these two species led to the identification of genes associated with leukocyte recruitment and germinal center formation. Conclusion: Our systems biology analysis of genome-wide expression data from salivary gland tissue of pSS patients and from a pSS mouse model identified common dysregulated biological pathways and molecular targets underlying critical molecular alterations in pSS pathogenesis
Self-adjustment mechanisms and their application for orthosis design
Medical orthoses aim at guiding anatomical joints along their natural trajectories while preventing pathological movements, especially in case of trauma or injuries. The motions that take place between bone surfaces have complex kinematics. These so-called arthrokinematic motions exhibit axes that move both in translation and rotation. Traditionally, orthoses are carefully adjusted and positioned such that their kinematics approximate the arthrokinematic movements as closely as possible in order to protect the joint. Adjustment procedures are typically long and tedious. We suggest in this paper another approach. We propose mechanisms having intrinsic self-aligning properties. They are designed such that their main axis self-adjusts with respect to the joint’s physiological axis during motion. When connected to a limb, their movement becomes homokinetic and they have the property of automatically minimizing internal stresses. The study is performed here in the planar case focusing on the most important component of the arthrokinematic motions of a knee joint
Resonances in and
A partial wave analysis is presented of and
from a sample of 58M events in the BES II detector. The
is observed clearly in both sets of data, and parameters of the
Flatt\' e formula are determined accurately: (stat)
(syst) MeV/c, MeV/c, . The data also exhibit a strong peak
centred at MeV/c. It may be fitted with and a
dominant signal made from interfering with a smaller
component. There is evidence that the signal is
resonant, from interference with . There is also a state in with MeV/c and
MeV/c; spin 0 is preferred over spin 2. This state, , is
distinct from . The data contain a strong peak due to
. A shoulder on its upper side may be fitted by interference
between and .Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.
Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0
Using 58 million J/psi and 14 million psi' decays obtained by the BESII
experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The
result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous
measurements.Comment: 9 pages, 8 figures, RevTex
Search for K_S K_L in psi'' decays
K_S K_L from psi'' decays is searched for using the psi'' data collected by
BESII at BEPC, the upper limit of the branching fraction is determined to be
B(psi''--> K_S K_L) < 2.1\times 10^{-4} at 90% C. L. The measurement is
compared with the prediction of the S- and D-wave mixing model of the
charmonia, based on the measurements of the branching fractions of J/psi-->K_S
K_L and psi'-->K_S K_L.Comment: 5 pages, 1 figur
First observation of psi(2S)-->K_S K_L
The decay psi(2S)-->K_S K_L is observed for the first time using psi(2S) data
collected with the Beijing Spectrometer (BESII) at the Beijing Electron
Positron Collider (BEPC); the branching ratio is determined to be
B(psi(2S)-->K_S K_L) = (5.24\pm 0.47 \pm 0.48)\times 10^{-5}. Compared with
J/psi-->K_S K_L, the psi(2S) branching ratio is enhanced relative to the
prediction of the perturbative QCD ``12%'' rule. The result, together with the
branching ratios of psi(2S) decays to other pseudoscalar meson pairs
(\pi^+\pi^- and K^+K^-), is used to investigate the relative phase between the
three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.Comment: 5 pages, 4 figures, 2 tables, submitted to Phys. Rev. Let
First Measurements of eta_c Decaying into K^+K^-2(pi^+pi^-) and 3(pi^+pi^-)
The decays of eta_c to K^+K^-2(pi^+pi^-) and 3(pi^+pi^-) are observed for the
first time using a sample of 5.8X10^7 J/\psi events collected by the BESII
detector. The product branching fractions are determined to be B(J/\psi-->gamma
eta_c)*B(eta_c-->K^+K^-pi^+pi^-pi^+pi^-)=(1.21+-0.32+-
0.23)X10^{-4}, and (J/\psi-->gamma eta_c)*
B(eta_c-->pi^+pi^-pi^+pi^-pi^+pi^-)= (2.59+-0.32+-0.48)X10^{-4}. The upper
limit for eta_c-->phi pi^+pi^-pi^+pi^- is also obtained as B(J/\psi-->gamma
eta_c)*B(eta_c--> phi pi^+pi^-pi^+pi^-)< 6.03 X10^{-5} at the 90% confidence
level.Comment: 11 pages, 4 figure
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