147 research outputs found
Computability of simple games: A characterization and application to the core
The class of algorithmically computable simple games (i) includes the class
of games that have finite carriers and (ii) is included in the class of games
that have finite winning coalitions. This paper characterizes computable games,
strengthens the earlier result that computable games violate anonymity, and
gives examples showing that the above inclusions are strict. It also extends
Nakamura's theorem about the nonemptyness of the core and shows that computable
games have a finite Nakamura number, implying that the number of alternatives
that the players can deal with rationally is restricted.Comment: 35 pages; To appear in Journal of Mathematical Economics; Appendix
added, Propositions, Remarks, etc. are renumbere
Controlling passively-quenched single photon detectors by bright light
Single photon detectors based on passively-quenched avalanche photodiodes can
be temporarily blinded by relatively bright light, of intensity less than a
nanowatt. I describe a bright-light regime suitable for attacking a quantum key
distribution system containing such detectors. In this regime, all single
photon detectors in the receiver Bob are uniformly blinded by continuous
illumination coming from the eavesdropper Eve. When Eve needs a certain
detector in Bob to produce a click, she modifies polarization (or other
parameter used to encode quantum states) of the light she sends to Bob such
that the target detector stops receiving light while the other detector(s)
continue to be illuminated. The target detector regains single photon
sensitivity and, when Eve modifies the polarization again, produces a single
click. Thus, Eve has full control of Bob and can do a successful
intercept-resend attack. To check the feasibility of the attack, 3 different
models of passively-quenched detectors have been tested. In the experiment, I
have simulated the intensity diagrams the detectors would receive in a real
quantum key distribution system under attack. Control parameters and side
effects are considered. It appears that the attack could be practically
possible.Comment: Experimental results from a third detector model added. Minor
corrections and edits made. 11 pages, 10 figure
Modeling the Effects of Cell Cycle M-phase Transcriptional Inhibition on Circadian Oscillation
Circadian clocks are endogenous time-keeping systems that temporally organize biological processes. Gating of cell cycle events by a circadian clock is a universal observation that is currently considered a mechanism serving to protect DNA from diurnal exposure to ultraviolet radiation or other mutagens. In this study, we put forward another possibility: that such gating helps to insulate the circadian clock from perturbations induced by transcriptional inhibition during the M phase of the cell cycle. We introduced a periodic pulse of transcriptional inhibition into a previously published mammalian circadian model and simulated the behavior of the modified model under both constant darkness and light–dark cycle conditions. The simulation results under constant darkness indicated that periodic transcriptional inhibition could entrain/lock the circadian clock just as a light–dark cycle does. At equilibrium states, a transcriptional inhibition pulse of certain periods was always locked close to certain circadian phases where inhibition on Per and Bmal1 mRNA synthesis was most balanced. In a light–dark cycle condition, inhibitions imposed at different parts of a circadian period induced different degrees of perturbation to the circadian clock. When imposed at the middle- or late-night phase, the transcriptional inhibition cycle induced the least perturbations to the circadian clock. The late-night time window of least perturbation overlapped with the experimentally observed time window, where mitosis is most frequent. This supports our hypothesis that the circadian clock gates the cell cycle M phase to certain circadian phases to minimize perturbations induced by the latter. This study reveals the hidden effects of the cell division cycle on the circadian clock and, together with the current picture of genome stability maintenance by circadian gating of cell cycle, provides a more comprehensive understanding of the phenomenon of circading gating of cell cycle
The origin of dust in galaxies revisited: the mechanism determining dust content
The origin of cosmic dust is a fundamental issue in planetary science. This
paper revisits the origin of dust in galaxies, in particular, in the Milky Way,
by using a chemical evolution model of a galaxy composed of stars, interstellar
medium, metals (elements heavier than helium), and dust. We start from a review
of time-evolutionary equations of the four components, and then, we present
simple recipes for the stellar remnant mass and yields of metal and dust based
on models of stellar nucleosynthesis and dust formation. After calibrating some
model parameters with the data from the solar neighborhood, we have confirmed a
shortage of the stellar dust production rate relative to the dust destruction
rate by supernovae if the destruction efficiency suggested by theoretical works
is correct. If the dust mass growth by material accretion in molecular clouds
is active, the observed dust amount in the solar neighborhood is reproduced. We
present a clear analytic explanation of the mechanism for determining dust
content in galaxies after the activation of accretion growth: a balance between
accretion growth and supernova destruction. Thus, the dust content is
independent of the uncertainty of the stellar dust yield after the growth
activation. The timing of the activation is determined by a critical metal mass
fraction which depends on the growth and destruction efficiencies. The solar
system formation seems to have occurred well after the activation and plenty of
dust would have existed in the proto-solar nebula.Comment: 12 pages, 11 figure
Using GIS to create synthetic disease outbreaks
BACKGROUND: The ability to detect disease outbreaks in their early stages is a key component of efficient disease control and prevention. With the increased availability of electronic health-care data and spatio-temporal analysis techniques, there is great potential to develop algorithms to enable more effective disease surveillance. However, to ensure that the algorithms are effective they need to be evaluated. The objective of this research was to develop a transparent user-friendly method to simulate spatial-temporal disease outbreak data for outbreak detection algorithm evaluation. A state-transition model which simulates disease outbreaks in daily time steps using specified disease-specific parameters was developed to model the spread of infectious diseases transmitted by person-to-person contact. The software was developed using the MapBasic programming language for the MapInfo Professional geographic information system environment. RESULTS: The simulation model developed is a generalised and flexible model which utilises the underlying distribution of the population and incorporates patterns of disease spread that can be customised to represent a range of infectious diseases and geographic locations. This model provides a means to explore the ability of outbreak detection algorithms to detect a variety of events across a large number of stochastic replications where the influence of uncertainty can be controlled. The software also allows historical data which is free from known outbreaks to be combined with simulated outbreak data to produce files for algorithm performance assessment. CONCLUSION: This simulation model provides a flexible method to generate data which may be useful for the evaluation and comparison of outbreak detection algorithm performance
The Cosmological Baryon Density from the Deuterium Abundance at a redshift z = 3.57
We present a measurement of the deuterium to hydrogen ratio in a quasar
absorption system at redshift z = 3.57 towards QSO 1937-1009. We use a two
component fit, with redshifts determined from unsaturated metal lines, to fit
the hydrogen and deuterium features simultaneously. We find a low value of D/H
= 2.3 \pm 0.6 \times 10^{-5}, which does not agree with other measurements of
high D/H (Songaila et al. 1994, Carswell et al. 1994). The absorption system is
very metal poor, with metallicities less than 1/100 solar. Standard models of
chemical evolution show the astration of deuterium is limited to a few percent
from primordial for systems this metal-poor, so we believe our value represents
the primordial one. Using predictions of standard big-bang nucleosynthesis and
measurements of the cosmic microwave background, our measurement gives the
density of baryons in units of the critical density, , where H_0 = 100 h km s^{-1] Mpc^{-1}.Comment: 10 pages, 2 Figures, also available at http://nately.ucsd.edu/ ;
submitted to Natur
Spatio-Temporal Transmission Patterns of Black-Band Disease in a Coral Community
Transmission mechanisms of black-band disease (BBD) in coral reefs are poorly understood, although this disease is considered to be one of the most widespread and destructive coral infectious diseases. The major objective of this study was to assess transmission mechanisms of BBD in the field based on the spatio-temporal patterns of the disease
Dynamic histone H3 methylation during gene induction: HYPB/Setd2 mediates all H3K36 trimethylation
Understanding the function of histone modifications across inducible genes in mammalian cells requires quantitative, comparative analysis of their fate during gene activation and identification of enzymes responsible. We produced high-resolution comparative maps of the distribution and dynamics of H3K4me3, H3K36me3, H3K79me2 and H3K9ac across c-fos and c-jun upon gene induction in murine fibroblasts. In unstimulated cells, continuous turnover of H3K9 acetylation occurs on all K4-trimethylated histone H3 tails; distribution of both modifications coincides across promoter and 5′ part of the coding region. In contrast, K36- and K79-methylated H3 tails, which are not dynamically acetylated, are restricted to the coding regions of these genes. Upon stimulation, transcription-dependent increases in H3K4 and H3K36 trimethylation are seen across coding regions, peaking at 5′ and 3′ ends, respectively. Addressing molecular mechanisms involved, we find that Huntingtin-interacting protein HYPB/Setd2 is responsible for virtually all global and transcription-dependent H3K36 trimethylation, but not H3K36-mono- or dimethylation, in these cells. These studies reveal four distinct layers of histone modification across inducible mammalian genes and show that HYPB/Setd2 is responsible for H3K36 trimethylation throughout the mouse nucleus
Chronic Exposure of Corals to Fine Sediments: Lethal and Sub-Lethal Impacts
Understanding the sedimentation and turbidity thresholds for corals is critical in assessing the potential impacts of dredging projects in tropical marine systems. In this study, we exposed two species of coral sampled from offshore locations to six levels of total suspended solids (TSS) for 16 weeks in the laboratory, including a 4 week recovery period. Dose-response relationships were developed to quantify the lethal and sub-lethal thresholds of sedimentation and turbidity for the corals. The sediment treatments affected the horizontal foliaceous species (Montipora aequituberculata) more than the upright branching species (Acropora millepora). The lowest sediment treatments that caused full colony mortality were 30 mg l−1 TSS (25 mg cm−2 day−1) for M. aequituberculata and 100 mg l−1 TSS (83 mg cm−2 day−1) for A. millepora after 12 weeks. Coral mortality generally took longer than 4 weeks and was closely related to sediment accumulation on the surface of the corals. While measurements of damage to photosystem II in the symbionts and reductions in lipid content and growth indicated sub-lethal responses in surviving corals, the most reliable predictor of coral mortality in this experiment was long-term sediment accumulation on coral tissue
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