A 750 mW, continuous-wave, solid-state laser source at 313 nm for cooling and manipulating trapped 9Be+ ions

We present a solid-state laser system that generates 750 mW of continuous-wave single-frequency output at 313 nm. Sum-frequency generation with fiber lasers at 1550 nm and 1051 nm produces up to 2 W at 626 nm. This visible light is then converted to UV by cavity-enhanced second-harmonic generation. The laser output can be tuned over a 495 GHz range, which includes the 9Be+ laser cooling and repumping transitions. This is the first report of a narrow-linewidth laser system with sufficient power to perform fault-tolerant quantum-gate operations with trapped 9Be+ ions by use of stimulated Raman transitions.Comment: 9 pages, 4 figure

Coherent master equation for laser modelocking

Modelocked lasers constitute the fundamental source of optically-coherent ultrashort-pulsed radiation, with huge impact in science and technology. Their modeling largely rests on the master equation (ME) approach introduced in 1975 by Hermann A. Haus. However, that description fails when the medium dynamics is fast and, ultimately, when light-matter quantum coherence is relevant. Here we set a rigorous and general ME framework, the coherent ME (CME), that overcomes both limitations. The CME predicts strong deviations from Haus ME, which we substantiate through an amplitude-modulated semiconductor laser experiment. Accounting for coherent effects, like the Risken-Nummedal-Graham-Haken multimode instability, we envisage the usefulness of the CME for describing self-modelocking and spontaneous frequency comb formation in quantum-cascade and quantum-dot lasers. Furthermore, the CME paves the way for exploiting the rich phenomenology of coherent effects in laser design, which has been hampered so far by the lack of a coherent ME formalism

Population based models of cortical drug response: insights from anaesthesia

A great explanatory gap lies between the molecular pharmacology of psychoactive agents and the neurophysiological changes they induce, as recorded by neuroimaging modalities. Causally relating the cellular actions of psychoactive compounds to their influence on population activity is experimentally challenging. Recent developments in the dynamical modelling of neural tissue have attempted to span this explanatory gap between microscopic targets and their macroscopic neurophysiological effects via a range of biologically plausible dynamical models of cortical tissue. Such theoretical models allow exploration of neural dynamics, in particular their modification by drug action. The ability to theoretically bridge scales is due to a biologically plausible averaging of cortical tissue properties. In the resulting macroscopic neural field, individual neurons need not be explicitly represented (as in neural networks). The following paper aims to provide a non-technical introduction to the mean field population modelling of drug action and its recent successes in modelling anaesthesia

A neural population model of the bi-phasic EEG-power spectrum during general anaesthesia

International audienceThe neuronal mechanisms of general anaesthesia are still poorly understood, though the induction of analgesia, amnesia, immobility and loss of consciousness by anaesthetic agents is well-established in hospital practice. To shed some light onto these mysterious effects, the chapter analyzes mathematically a neural field model describing the neural population dynamics by an integro-differential equation. The power spectrum is derived and compared to experimental results

Quantitative electroencephalographic analysis of the biphasic concentration-effect relationship of propofol in surgical patients during extradural analgesia

We studied effects on the EEG of propofol infused at a rate of 0.5 mg kg(-1) min(-1) for 10 min in 10 healthy male surgical patients under extradural analgesia. The EEG amplitude in six frequency bands was related to arterial blood propofol concentrations and responsiveness to verbal commands. The EEG amplitude showed a characteristic biphasic response to increasing blood propofol concentrations in all frequency bands. During the infusion, patients lost responsiveness when EEG amplitudes in the high frequency bands were decreasing after having reached a maximum. EEG changes were different during infusion and emergence. Pharmacodynamic modelling, using two effect compartments with dissimilar equilibration constants, resulted in satisfactory fits. We conclude that propofol exerts a biphasic effect on the EEG amplitude in all frequency bands. The dissimilarity of EEG changes during infusion and during emergence suggests that two effect compartments with different equilibration constants exert opposing effects on the EEG

Quantitative electroencephalographic analysis of the biphasic concentration-effect relationship of propofol in surgical patients during extradural analgesia

We studied effects on the EEG of propofol infused at a rate of 0.5 mg kg(-1) min(-1) for 10 min in 10 healthy male surgical patients under extradural analgesia. The EEG amplitude in six frequency bands was related to arterial blood propofol concentrations and responsiveness to verbal commands. The EEG amplitude showed a characteristic biphasic response to increasing blood propofol concentrations in all frequency bands. During the infusion, patients lost responsiveness when EEG amplitudes in the high frequency bands were decreasing after having reached a maximum. EEG changes were different during infusion and emergence. Pharmacodynamic modelling, using two effect compartments with dissimilar equilibration constants, resulted in satisfactory fits. We conclude that propofol exerts a biphasic effect on the EEG amplitude in all frequency bands. The dissimilarity of EEG changes during infusion and during emergence suggests that two effect compartments with different equilibration constants exert opposing effects on the EEG.</p

Biphasic EEG changes in relation to loss of consciousness during induction with thiopental, propofol, etomidate, midazolam or sevoflurane

The time course of four EEG effect variables, amplitude in the 2-5 Hz and in the 11-15 Hz band, spectral edge frequency 95% (SEF95), and bispectral index (BIS), in response to increasing concentrations of thiopental, propofol, etomidate, midazolam, or sevoflurane during a 10 min induction of anaesthesia was studied in 25 patients to determine the existence of a biphasic effect and to study the relationship of the EEG effect to the moment of loss of consciousness. A biphasic effect, that is, an initial increase of the effect variable followed by a decrease at higher concentrations, during the transition from consciousness to unconsciousness was found in EEG amplitude (both frequency bands) and in SEF95 for all anaesthetics except midazolam. There was a concentration-related decrease in BIS for all anaesthetics. There was no consistent relationship between the time of occurrence of the peak EEG effect, or the value of the EEG variable and the moment of loss of consciousness. With rapidly changing drug concentrations during the induction of anaesthesia, none of these EEG effect variables could be correlated to the moment of loss of consciousness