235 research outputs found
Tight Competitive Analyses of Online Car-Sharing Problems
The car-sharing problem, proposed by Luo, Erlebach and Xu in 2018, mainly
focuses on an online model in which there are two locations: 0 and 1, and
total cars. Each request which specifies its pick-up time and pick-up location
(among 0 and 1, and the other is the drop-off location) is released in each
stage a fixed amount of time before its specified start (i.e. pick-up) time.
The time between the booking (i.e. released) time and the start time is enough
to move empty cars between 0 and 1 for relocation if they are not used in that
stage. The model, called S2L-F, assumes that requests in each stage arrive
sequentially regardless of the same booking time and the decision (accept or
reject) must be made immediately. The goal is to accept as many requests as
possible. In spite of only two locations, the analysis does not seem easy and
the (tight) competitive ratio (CR) is only known to be 2.0 for and 1.5
for a restricted value of , i.e., a multiple of three. In this paper, we
remove all the holes of unknown CR's; namely we prove that the CR is
for all . Furthermore, if the
algorithm can delay its decision until all requests have come in each stage,
the CR is improved to roughly 4/3. We can take this advantage even further,
precisely we can achieve a CR of if the number of requests in
each stage is at most , , where we do not have to know the
value of in advance. Finally we demonstrate that randomization also helps
to get (slightly) better CR's
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α-Lactosylceramide Protects Against iNKT-Mediated Murine Airway Hyperreactivity and Liver Injury Through Competitive Inhibition of Cd1d Binding.
Invariant natural killer T (iNKT) cells, which are activated by T cell receptor (TCR)-dependent recognition of lipid-based antigens presented by the CD1d molecule, have been shown to participate in the pathogenesis of many diseases, including asthma and liver injury. Previous studies have shown the inhibition of iNKT cell activation using lipid antagonists can attenuate iNKT cell-induced disease pathogenesis. Hence, the development of iNKT cell-targeted glycolipids can facilitate the discovery of new therapeutics. In this study, we synthesized and evaluated α-lactosylceramide (α-LacCer), an α-galactosylceramide (α-GalCer) analog with lactose substitution for the galactose head and a shortened acyl chain in the ceramide tail, toward iNKT cell activation. We demonstrated that α-LacCer was a weak inducer for both mouse and human iNKT cell activation and cytokine production, and the iNKT induction by α-LacCer was CD1d-dependent. However, when co-administered with α-GalCer, α-LacCer inhibited α-GalCer-induced IL-4 and IFN-γ production from iNKT cells. Consequently, α-LacCer also ameliorated both α-GalCer and GSL-1-induced airway hyperreactivity and α-GalCer-induced neutrophilia when co-administered in vivo. Furthermore, we were able to inhibit the increases of ConA-induced AST, ALT and IFN-γ serum levels through α-LacCer pre-treatment, suggesting α-LacCer could protect against ConA-induced liver injury. Mechanistically, we discerned that α-LacCer suppressed α-GalCer-stimulated cytokine production through competing for CD1d binding. Since iNKT cells play a critical role in the development of AHR and liver injury, the inhibition of iNKT cell activation by α-LacCer present a possible new approach in treating iNKT cell-mediated diseases
Dendrobium officinale
Background. Dendrobium officinale (DO) Kimura et Migo is a precious Chinese herb that is considered beneficial for health due to its antioxidant and antidiabetes properties, and so on. In this research, we try to determine the preventive effect of DO on the early complications of STZ-induced diabetic rats. Methods. Type 1 diabetic rats were produced with a single intraperitoneal injection of STZ (50 mg/kg). DO (1 g/kg/day) was then orally administered for 5 weeks. Blood glucose, TC, TG, BUN, CREA, and GSH-PX levels were determined, and electroretinographic activity and hypoalgesia were investigated. Pathological sections of the eyes, hearts, aortas, kidneys, and livers were analyzed. Results. Treatment with DO significantly attenuated the serum levels of TC, TG, BUN, and CREA, markedly increased the amplitudes of ERG a- and b-waves and Ops, and reduced the hypoalgesia and histopathological changes of vital organs induced by hyperglycemia. The protective effect of DO in diabetic rats may be associated with its antioxidant activity, as evidenced by the marked increase in the serum level of glutathione peroxidase. However, DO had no significant effect on blood glucose levels and bodyweight of diabetic rats. Conclusions. DO supplementation is an effective treatment to prevent STZ-induced diabetic complications
Inhibition of Anchorage-Independent Proliferation and G0/G1 Cell-Cycle Regulation in Human Colorectal Carcinoma Cells by 4,7-Dimethoxy-5-Methyl-l,3-Benzodioxole Isolated from the Fruiting Body of Antrodia camphorate
In this study, 4,7-dimethoxy-5-methyl-l,3-benzodioxole (SY-1) was isolated from three different sources of dried fruiting bodies of Antrodia camphorate (AC). AC is a medicinal mushroom that grows on the inner heartwood wall of Cinnamomum kanehirai Hay (Lauraceae), an endemic species that is used in Chinese medicine for its anti-tumor and immunomodulatory properties. In this study, we demonstrated that SY-1 profoundly decreased the proliferation of human colon cancer cells (COLO 205) through G0/G1 cell-cycle arrest (50–150 μM) and induction of apoptosis (>150 μM). Cell-cycle arrest induced by SY-1 was associated with a significant increase in levels of p53, p21/Cip1 and p27/Kip1, and a decrease in cyclins D1, D3 and A. In contrast, SY-1 treatment did not induce significant changes in G0/G1 phase cell-cycle regulatory proteins in normal human colonic epithelial cells (FHC). The cells were cultured in soft agar to evaluate anchorage-independent colony formation, and we found that the number of transformed colonies was significantly reduced in the SY-1-treated COLO 205 cells. These findings demonstrate for the first time that SY-1 inhibits human colon cancer cell proliferation through inhibition of cell growth and anchorage-independent colony formation in soft agar. However, the detailed mechanisms of these processes remain unclear and will require further investigation
Local Magnetic Field Role in Star Formation
We highlight distinct and systematic observational features of magnetic field
morphologies in polarized submm dust continuum. We illustrate this with
specific examples and show statistical trends from a sample of 50 star-forming
regions.Comment: 4 pages, 3 figures; to appear in the EAS Proceedings of the 6th
Zermatt ISM Symposium "Conditions and Impact of Star Formation from Lab to
Space", September 201
Magnetic Fields and Massive Star Formation
Massive stars ( \msun) typically form in parsec-scale molecular clumps
that collapse and fragment, leading to the birth of a cluster of stellar
objects. We investigate the role of magnetic fields in this process through
dust polarization at 870 m obtained with the Submillimeter Array (SMA).
The SMA observations reveal polarization at scales of \lsim 0.1 pc. The
polarization pattern in these objects ranges from ordered hour-glass
configurations to more chaotic distributions. By comparing the SMA data with
the single dish data at parsec scales, we found that magnetic fields at dense
core scales are either aligned within of or perpendicular to the
parsec-scale magnetic fields. This finding indicates that magnetic fields play
an important role during the collapse and fragmentation of massive molecular
clumps and the formation of dense cores. We further compare magnetic fields in
dense cores with the major axis of molecular outflows. Despite a limited number
of outflows, we found that the outflow axis appears to be randomly oriented
with respect to the magnetic field in the core. This result suggests that at
the scale of accretion disks (\lsim 10^3 AU), angular momentum and dynamic
interactions possibly due to close binary or multiple systems dominate over
magnetic fields. With this unprecedentedly large sample massive clumps, we
argue on a statistical basis that magnetic fields play an important role during
the formation of dense cores at spatial scale of 0.01 - 0.1 pc in the context
of massive star and cluster star formation.Comment: Accepted for publication in Astrophysical Journa
Multi-scale physical properties of NGC 6334 as revealed by local relative orientations between magnetic fields, density gradients, velocity gradients, and gravity
We present ALMA dust polarization and molecular line observations toward 4
clumps (I(N), I, IV, and V) in the massive star-forming region NGC 6334. In
conjunction with large-scale dust polarization and molecular line data from
JCMT, Planck, and NANTEN2, we make a synergistic analysis of relative
orientations between magnetic fields (), column density
gradients (), local gravity (), and
velocity gradients () to investigate the multi-scale
(from 30 pc to 0.003 pc) physical properties in NGC 6334. We find that
the relative orientation between and
changes from statistically more perpendicular to
parallel as column density () increases, which is a signature
of trans-to-sub-Alfv\'{e}nic turbulence at complex/cloud scales as revealed by
previous numerical studies. Because and
are preferentially aligned within the NGC 6334 cloud, we
suggest that the more parallel alignment between and
at higher is because the magnetic
field line is dragged by gravity. At even higher , the angle
between and or
transits back to having no preferred orientation or
statistically slightly more perpendicular, suggesting that the magnetic field
structure is impacted by star formation activities. A statistically more
perpendicular alignment is found between and
throughout our studied range, which
indicates a trans-to-sub-Alfv\'{e}nic state at small scales as well. The
normalised mass-to-flux ratio derived from the polarization-intensity gradient
(KTH) method increases with .Comment: 35 pages, 18 figures. Accepted by Ap
The Relation Between Brain Amyloid Deposition, Cortical Atrophy, and Plasma Biomarkers in Amnesic Mild Cognitive Impairment and Alzheimer’s Disease
Background: Neuritic plaques and neurofibrillary tangles are the pathological hallmarks of Alzheimer’s disease (AD), while the role of brain amyloid deposition in the clinical manifestation or brain atrophy remains unresolved. We aimed to explore the relation between brain amyloid deposition, cortical thickness, and plasma biomarkers.Methods: We used 11C-Pittsburgh compound B-positron emission tomography to assay brain amyloid deposition, magnetic resonance imaging to estimate cortical thickness, and an immunomagnetic reduction assay to measure plasma biomarkers. We recruited 39 controls, 25 subjects with amnesic mild cognitive impairment (aMCI), and 16 subjects with AD. PiB positivity (PiB+) was defined by the upper limit of the 95% confidence interval of the mean cortical SUVR from six predefined regions (1.0511 in this study).Results: All plasma biomarkers showed significant between-group differences. The plasma Aβ40 level was positively correlated with the mean cortical thickness of both the PiB+ and PiB- subjects. The plasma Aβ40 level of the subjects who were PiB+ was negatively correlated with brain amyloid deposition. In addition, the plasma tau level was negatively correlated with cortical thickness in both the PiB+ and PiB- subjects. Moreover, cortical thickness was negatively correlated with brain amyloid deposition in the PiB+ subjects. In addition, the cut-off point of plasma tau for differentiating between controls and AD was higher in the PiB- group than in the PiB+ group (37.5 versus 25.6 pg/ml, respectively). Lastly, ApoE4 increased the PiB+ rate in the aMCI and control groups.Conclusion: The contributions of brain amyloid deposition to cortical atrophy are spatially distinct. Plasma Aβ40 might be a protective indicator of less brain amyloid deposition and cortical atrophy. It takes more tau pathology to reach the same level of cognitive decline in subjects without brain amyloid deposition, and ApoE4 plays an early role in amyloid pathogenesis
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