Measuring entanglement of photons produced by a pulsed source

A pulsed source of entangled photons is desirable for some applications. Yet, such a source has intrinsic problems arising from the simultaneous arrival of the signal and noise photons to the detectors. These problems are analyzed and practical methods to calculate the number of accidental (or spurious) coincidences are described in detail, and experimentally checked, for the different regimes of interest. The results are useful not only to measure entanglement, but to all the situations where extracting the number of valid coincidences from noisy data is required. As an example of the use of those methods, we present the time-resolved measurement of the Concurrence of the field produced by spontaneous parametric down conversion with pump pulses of duration in the ns-range at a repetition of kHz. The predicted discontinuous evolution of the entanglement at the edges of the pump pulse is observed.Comment: 9 pages, 10 or 7 figures (one of the figures includes 4), 28 Refernce

The open XXZ and associated models at q root of unity

The generalized open XXZ model at $q$ root of unity is considered. We review how associated models, such as the $q$ harmonic oscillator, and the lattice sine-Gordon and Liouville models are obtained. Explicit expressions of the local Hamiltonian of the spin ${1 \over 2}$ XXZ spin chain coupled to dynamical degrees of freedom at the one end of the chain are provided. Furthermore, the boundary non-local charges are given for the lattice sine Gordon model and the $q$ harmonic oscillator with open boundaries. We then identify the spectrum and the corresponding Bethe states, of the XXZ and the q harmonic oscillator in the cyclic representation with special non diagonal boundary conditions. Moreover, the spectrum and Bethe states of the lattice versions of the sine-Gordon and Liouville models with open diagonal boundaries is examined. The role of the conserved quantities (boundary non-local charges) in the derivation of the spectrum is also discussed.Comment: 31 pages, LATEX, minor typos correcte

Пневмонии и их диагностика в стационарах Санкт-Петербурга по данным аутопсий

15 633 records of postmortem examinations of the St.-Petersburg municipal bureaus were analyzed for 1993— 1995. All kinds of pneumonia were revealed in 38% of cases. The frequency of primary and secondary pneumonia including pneumonia as a manifestation of chronic bronchitis exacerbation, was analyzed. The low quality of pneumonia diagnosis in non-specialized hospitals as well as its reasons are shown.Проанализированы 15 633 протокола патологоанатомических вскрытий городского бюро Санкт-Петербурга за 1993—1995 гг. Выявлено, что все виды пневмоний обнаружены в 38% наблюдений. Проанализирована частота первичных и вторичных пневмоний, а также пневмоний, явившихся проявлением обострения хронического бронхита. Показан низкий уровень диагностики пневмоний в стационарах общего профиля и его причины

Ion Channel Density Regulates Switches between Regular and Fast Spiking in Soma but Not in Axons

The threshold firing frequency of a neuron is a characterizing feature of its dynamical behaviour, in turn determining its role in the oscillatory activity of the brain. Two main types of dynamics have been identified in brain neurons. Type 1 dynamics (regular spiking) shows a continuous relationship between frequency and stimulation current (f-Istim) and, thus, an arbitrarily low frequency at threshold current; Type 2 (fast spiking) shows a discontinuous f-Istim relationship and a minimum threshold frequency. In a previous study of a hippocampal neuron model, we demonstrated that its dynamics could be of both Type 1 and Type 2, depending on ion channel density. In the present study we analyse the effect of varying channel density on threshold firing frequency on two well-studied axon membranes, namely the frog myelinated axon and the squid giant axon. Moreover, we analyse the hippocampal neuron model in more detail. The models are all based on voltage-clamp studies, thus comprising experimentally measurable parameters. The choice of analysing effects of channel density modifications is due to their physiological and pharmacological relevance. We show, using bifurcation analysis, that both axon models display exclusively Type 2 dynamics, independently of ion channel density. Nevertheless, both models have a region in the channel-density plane characterized by an N-shaped steady-state current-voltage relationship (a prerequisite for Type 1 dynamics and associated with this type of dynamics in the hippocampal model). In summary, our results suggest that the hippocampal soma and the two axon membranes represent two distinct kinds of membranes; membranes with a channel-density dependent switching between Type 1 and 2 dynamics, and membranes with a channel-density independent dynamics. The difference between the two membrane types suggests functional differences, compatible with a more flexible role of the soma membrane than that of the axon membrane

Doubly heavy baryons Omega_QQ' vs. Xi_QQ' in sum rules of NRQCD

In the framework of two-point sum rules of NRQCD, the masses and couplings of doubly heavy baryons to the corresponding quark currents are evaluated with account of coulomb-like corrections in the system of doubly heavy diquark as well as the contribution of nonperturbative terms determined by the quark, gluon, mixed condensates and the product of gluon and quark condensates. The introduction of nonzero light quark mass destroys the factorization of baryon and diquark correlators even at the perturbative level and provides the better convergency of sum rules. We estimate the difference M_Omega - M_Xi = 100+/- 10 MeV. The ratio of baryonic constants |Z_Omega|^2/|Z_Xi|^2 is equal to 1.3+/-0.2 indicating the violation of SU(3) flavor symmetry for the doubly heavy baryons.Comment: 18 pages, ReVTeX file, 7 eps-figures, references adde

Identification of Molecular Pathologies Sufficient to Cause Neuropathic Excitability in Primary Somatosensory Afferents Using Dynamical Systems Theory

Pain caused by nerve injury (i.e. neuropathic pain) is associated with development of neuronal hyperexcitability at several points along the pain pathway. Within primary afferents, numerous injury-induced changes have been identified but it remains unclear which molecular changes are necessary and sufficient to explain cellular hyperexcitability. To investigate this, we built computational models that reproduce the switch from a normal spiking pattern characterized by a single spike at the onset of depolarization to a neuropathic one characterized by repetitive spiking throughout depolarization. Parameter changes that were sufficient to switch the spiking pattern also enabled membrane potential oscillations and bursting, suggesting that all three pathological changes are mechanistically linked. Dynamical analysis confirmed this prediction by showing that excitability changes co-develop when the nonlinear mechanism responsible for spike initiation switches from a quasi-separatrix-crossing to a subcritical Hopf bifurcation. This switch stems from biophysical changes that bias competition between oppositely directed fast- and slow-activating conductances operating at subthreshold potentials. Competition between activation and inactivation of a single conductance can be similarly biased with equivalent consequences for excitability. “Bias” can arise from a multitude of molecular changes occurring alone or in combination; in the latter case, changes can add or offset one another. Thus, our results identify pathological change in the nonlinear interaction between processes affecting spike initiation as the critical determinant of how simple injury-induced changes at the molecular level manifest complex excitability changes at the cellular level. We demonstrate that multiple distinct molecular changes are sufficient to produce neuropathic changes in excitability; however, given that nerve injury elicits numerous molecular changes that may be individually sufficient to alter spike initiation, our results argue that no single molecular change is necessary to produce neuropathic excitability. This deeper understanding of degenerate causal relationships has important implications for how we understand and treat neuropathic pain

Rheumatic heart disease and enteroviruses

In material from 1086 patients who underwent heart valve disease surgery, traditional hystologic assessment, argyrophilic nucleolar organizer analysis, with calculation of mean Ag granule number per endotheliocyte and fibroblast nucleus; immuno-hystochemical assay with monoclone antibodies to Enteroviruses, vimentin, desmin, SMA, SMA, Ki-67-, bcl-2-antigens; print-smear cytology; and valve PCR were performed. Enterovirus replication was observed in endotheliocytes, fibroblasts, and smooth muscle cells in all cases of active rheumatism. Endothelial dysfunction was associated with Enterovirus infection