1,640 research outputs found

    Airborne Advanced Reconfigurable Computer System (ARCS)

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    A digital computer subsystem fault-tolerant concept was defined, and the potential benefits and costs of such a subsystem were assessed when used as the central element of a new transport's flight control system. The derived advanced reconfigurable computer system (ARCS) is a triple-redundant computer subsystem that automatically reconfigures, under multiple fault conditions, from triplex to duplex to simplex operation, with redundancy recovery if the fault condition is transient. The study included criteria development covering factors at the aircraft's operation level that would influence the design of a fault-tolerant system for commercial airline use. A new reliability analysis tool was developed for evaluating redundant, fault-tolerant system availability and survivability; and a stringent digital system software design methodology was used to achieve design/implementation visibility

    Quantum critical behavior in the heavy Fermion single crystal Ce(Ni0.935_{0.935}Pd0.065_{0.065})2_2Ge2_2

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    We have performed magnetic susceptibility, specific heat, resistivity, and inelastic neutron scattering measurements on a single crystal of the heavy Fermion compound Ce(Ni0.935_{0.935}Pd0.065_{0.065})2_2Ge2_2, which is believed to be close to a quantum critical point (QCP) at T = 0. At lowest temperature(1.8-3.5 K), the magnetic susceptibility behaves as χ(T)χ(0)\chi(T)-\chi (0) \propto T1/6T^{-1/6} with χ(0)=0.032×106\chi (0) = 0.032 \times 10^{-6} m3^3/mole (0.0025 emu/mole). For T<T< 1 K, the specific heat can be fit to the formula ΔC/T=γ0T1/2\Delta C/T = \gamma_0 - T^{1/2} with γ0\gamma_0 of order 700 mJ/mole-K2^2. The resistivity behaves as ρ=ρ0+AT3/2\rho = \rho_0 + AT^{3/2} for temperatures below 2 K. This low temperature behavior for γ(T)\gamma (T) and ρ(T)\rho (T) is in accord with the SCR theory of Moriya and Takimoto\cite{Moriya}. The inelastic neutron scattering spectra show a broad peak near 1.5 meV that appears to be independent of QQ; we interpret this as Kondo scattering with TK=T_K = 17 K. In addition, the scattering is enhanced near QQ=(1/2, 1/2, 0) with maximum scattering at ΔE\Delta E = 0.45 meV; we interpret this as scattering from antiferromagnetic fluctuations near the antiferromagnetic QCP.Comment: to be published in J. Phys: Conference Serie

    Strategic Shift to a Diagnostic Model of Care in a Multi-Site Group Dental Practice.

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    BackgroundDocumenting standardized dental diagnostic terms represents an emerging change for how dentistry is practiced. We focused on a mid-sized dental group practice as it shifted to a policy of documenting patients' diagnoses using standardized terms in the electronic health record.MethodsKotter's change framework was translated into interview questions posed to the senior leadership in a mid-size dental group practice. In addition, quantitative content analyses were conducted on the written policies and forms before and after the implementation of standardized diagnosis documentation to assess the extent to which the forms and policies reflected the shift. Three reviewers analyzed the data individually and reached consensuses where needed.ResultsKotter's guiding change framework explained the steps taken to 97 percent utilization rate of the Electronic Health Record and Dental Diagnostic Code. Of the 96 documents included in the forms and policy analysis, 31 documents were officially updated but only two added a diagnostic element.ConclusionChange strategies established in the business literature hold utility for dental practices seeking diagnosis-centered care.Practical implicationsA practice that shifts to a diagnosis-driven care philosophy would be best served by ensuring that the change process follows a leadership framework that is calibrated to the organization's culture

    Stimulation of Adenosine A 3 Receptors in Cerebral Ischemia: Neuronal Death, Recovery, or Both?

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    The role of the adenosine A 3 receptor continues to baffle, and, despite an increasing number of studies, the currently available data add to, rather than alleviate, the existing confusion. The reported effects of adenosine A 3 receptor stimulation appear to depend on the pattern of drug administration (acute vs. chronic), dose, and type of the target tissue. Thus, while acute exposure to A 3 receptor agonists protects against myocardial ischemia, it is severely damaging when these agents are given shortly prior to cerebral ischemia. Mast cells degranulate when their A 3 receptors are stimulated. Degranulation of neutrophils is, on the other hand, impaired. While reduced production of reactive nitrogen species has been reported following activation of A 3 receptors in collagen-induced arthritis, the process appears to be enhanced in cerebral ischemia. Indeed, immunocytochemical studies indicate that both pre- and postischemic treatment with A 3 receptor antagonist dramatically reduces nitric oxide synthase in the affected hippocampus. Even more surprisingly, low doses of A 3 receptor agonists seem to enhance astrocyte proliferation, while high doses induce their apoptosis. This review concentrates on the studies of cerebral A 3 receptors and, based on the available evidence, discusses the possibility of adenosine A 3 receptor serving as an integral element of the endogenous cerebral neuroprotective complex consisting of adenosine and its receptors.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75391/1/j.1749-6632.1999.tb07984.x.pd
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