Satisfiability of CTL* with constraints

We show that satisfiability for CTL* with equality-, order-, and modulo-constraints over Z is decidable. Previously, decidability was only known for certain fragments of CTL*, e.g., the existential and positive fragments and EF.Comment: To appear at Concur 201

Equivelar and d-Covered Triangulations of Surfaces. I

We survey basic properties and bounds for $q$-equivelar and $d$-covered triangulations of closed surfaces. Included in the survey is a list of the known sources for $q$-equivelar and $d$-covered triangulations. We identify all orientable and non-orientable surfaces $M$ of Euler characteristic $0>\chi(M)\geq -230$ which admit non-neighborly $q$-equivelar triangulations with equality in the upper bound $q\leq\Bigl\lfloor\tfrac{1}{2}(5+\sqrt{49-24\chi (M)})\Bigl\rfloor$. These examples give rise to $d$-covered triangulations with equality in the upper bound $d\leq2\Bigl\lfloor\tfrac{1}{2}(5+\sqrt{49-24\chi (M)})\Bigl\rfloor$. A generalization of Ringel's cyclic $7{\rm mod}12$ series of neighborly orientable triangulations to a two-parameter family of cyclic orientable triangulations $R_{k,n}$, $k\geq 0$, $n\geq 7+12k$, is the main result of this paper. In particular, the two infinite subseries $R_{k,7+12k+1}$ and $R_{k,7+12k+2}$, $k\geq 1$, provide non-neighborly examples with equality for the upper bound for $q$ as well as derived examples with equality for the upper bound for $d$.Comment: 21 pages, 4 figure

Constraint checking during error recovery

The system-level software onboard a spacecraft is responsible for recovery from communication, power, thermal, and computer-health anomalies that may occur. The recovery must occur without disrupting any critical scientific or engineering activity that is executing at the time of the error. Thus, the error-recovery software may have to execute concurrently with the ongoing acquisition of scientific data or with spacecraft maneuvers. This work provides a technique by which the rules that constrain the concurrent execution of these processes can be modeled in a graph. An algorithm is described that uses this model to validate that the constraints hold for all concurrent executions of the error-recovery software with the software that controls the science and engineering activities of the spacecraft. The results are applicable to a variety of control systems with critical constraints on the timing and ordering of the events they control

Towards automation of user interface design

This paper suggests an approach to automatic software design in the domain of graphical user interfaces. There are still some drawbacks in existing user interface management systems (UIMS's) which basically offer only quantitative layout specifications via direct manipulation. Our approach suggests a convenient way to get a default graphical user interface which may be customized and redesigned easily in further prototyping cycles

On finite volume effects in the chiral extrapolation of baryon masses

We perform an analysis of the QCD lattice data on the baryon octet and decuplet masses based on the relativistic chiral Lagrangian. The baryon self energies are computed in a finite volume at next-to-next-to-next-to leading order (N$^3$LO), where the dependence on the physical meson and baryon masses is kept. The number of free parameters is reduced significantly down to 12 by relying on large-$N_c$ sum rules. Altogether we describe accurately more than 220 data points from six different lattice groups, BMW, PACS-CS, HSC, LHPC, QCDSF-UKQCD and NPLQCD. Values for all counter terms relevant at N$^3$LO are predicted. In particular we extract a pion-nucleon sigma term of 39$_{-1}^{+2}$ MeV and a strangeness sigma term of the nucleon of $\sigma_{sN} = 84^{+ 28}_{-\;4}$ MeV. The flavour SU(3) chiral limit of the baryon octet and decuplet masses is determined with $(802 \pm 4)$ MeV and $(1103 \pm 6)$ MeV. Detailed predictions for the baryon masses as currently evaluated by the ETM lattice QCD group are made.Comment: 44 pages, 10 figures and 6 tables - the revised manuscript contains the results of additional fits at the N^2LO level - 4 additional figures show the size of finite volume corrections for each lattice point - more technical details on the evaluation of finite volume effects are give

Dose-response relationship and low dose extrapolatioin in chemical carcinogenesis

Data supporting various dose-response relationships in chemical carcinogenesis are summarized. General principles are derived to explain the relationships between exposure dose, DNA adduct level, induction of genetic changes, and tumor incidence. Some mechanistic aspects of epigenetic carcinogens (stimulation of cell division and maldifferentiation) are analyzed in a similar way. In a homogeneous population, non-linearities are frequent. They are due to phenomena of induction or saturation of enzymatic activities and to the multi-step nature of carcinogenesis: if a carcinogen accelerates more than one step, the superposition of the dose-response curves for the individual steps can result in an exponential relationship. A fourth power of the dose was the maximum seen in animals (formaldehyde). At the lowest dose levels, a proportionality between dose and tumor induction is postulated independent of the mechanism of action if the carcinogen accelerates the endogenous process responsible for spontaneous tumor formation. Low-dose thresholds are expected only for situations where the carcinogen acts in a way that has no endogenous counterpart. Epidemlological studies in humans show linear dose-response curves in all but two investigations. The difference from the strongly non-linear slopes seen in animal studies could be due to the heterogeneity of the human population: if the individual sensitivity to a carcinogen is governed by a large number of genetic and life-style factors, the non-linearities will tend to cancel each other out and the dose-response curve becomes ‘quasi-linear

Critical role of canonical transient receptor potential channel 7 in initiation of seizures

Status epilepticus (SE) is a life-threatening disease that has been recognized since antiquity but still causes over 50,000 deaths annually in the United States. The prevailing view on the pathophysiology of SE is that it is sustained by a loss of normal inhibitory mechanisms of neuronal activity. However, the early process leading to the initiation of SE is not well understood. Here, we show that, as seen in electroencephalograms, SE induced by the muscarinic agonist pilocarpine in mice is preceded by a specific increase in the gamma wave, and genetic ablation of canonical transient receptor potential channel (TRPC) 7 significantly reduces this pilocarpine-induced increase of gamma wave activity, preventing the occurrence of SE. At the cellular level, TRPC7 plays a critical role in the generation of spontaneous epileptiform burst firing in cornu ammonis (CA) 3 pyramidal neurons in brain slices. At the synaptic level, TRPC7 plays a significant role in the long-term potentiation at the CA3 recurrent collateral synapses and Schaffer collateral-CA1 synapses, but not at the mossy fiber-CA3 synapses. Taken together, our data suggest that epileptiform burst firing generated in the CA3 region by activity-dependent enhancement of recurrent collateral synapses may be an early event in the initiation process of SE and that TRPC7 plays a critical role in this cellular event. Our findings reveal that TRPC7 is intimately involved in the initiation of seizures both in vitro and in vivo. To our knowledge, this contribution to initiation of seizures is the first identified functional role for the TRPC7 ion channel.Fil: Phelan, K. D.. University of Arkansas for Medical Sciences; Estados UnidosFil: Shwe, U. T.. University of Arkansas for Medical Sciences; Estados UnidosFil: Abramowitz, J.. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados UnidosFil: Zheng, F.. University of Arkansas for Medical Sciences; Estados Unido