Compensating fictitious magnetic field gradients in optical microtraps by using elliptically polarized dipole light

Tightly focused optical dipole traps induce vector light shifts ("fictitious magnetic fields") which complicate their use for single-atom trapping and manipulation. The problem can be mitigated by adding a larger, real magnetic field, but this solution is not always applicable; in particular, it precludes fast switching to a field-free configuration. Here we show that this issue can be addressed elegantly by deliberately adding a small elliptical polarization component to the dipole beam. In our experiments with single $^{87}$Rb atoms in a chopped trap, we observe improvements up to a factor 11 of the trap lifetime compared to the standard, seemingly ideal linear polarization. This effect results from a modification of heating processes via spin-state diffusion in state-dependent trapping potentials. We develop Monte-Carlo simulations of the evolution of the atom's internal and motional states and find that they agree quantitatively with the experimental data. The method is general and can be applied in all experiments where the longitudinal polarization component is non-negligible.Comment: 6 pages, 5 figure

Overlapping two standing-waves in a microcavity for a multi-atom photon interface

We develop a light-matter interface enabling strong and uniform coupling between a chain of cold atoms and photons of an optical cavity. This interface is a fiber Fabry-Perot cavity, doubly resonant for both the wavelength of the atomic transition and for a geometrically commensurate red-detuned intracavity trapping lattice. Fulfilling the condition of a strong and uniform atom-photon coupling requires optimization of the spatial overlap between the two standing waves in the cavity. In a strong-coupling cavity, where the mode waists and Rayleigh range are small, we derive the expression of the optimal trapping wavelength taking into account the Gouy phase. The main parameter controlling the overlap of the standing waves is the relative phase shift at the reflection on the cavity mirrors between the two wavelengths, for which we derive the optimal value. We have built a microcavity optimized according to these results, employing custom-made mirrors with engineered reflection phase for both wavelengths. We present a method to measure with high precision the relative phase shift at reflection, which allows us to determine the spatial overlap of the two modes in this cavity.Comment: 14 pages, 7 figure

Millimeter-long Fiber Fabry-Perot cavities

We demonstrate fiber Fabry-Perot (FFP) cavities with concave mirrors that can be operated at cavity lengths as large as 1.5mm without significant deterioration of the finesse. This is achieved by using a laser dot machining technique to shape spherical mirrors with ultralow roughness and employing single-mode fibers with large mode area for good mode matching to the cavity. Additionally, in contrast to previous FFPs, these cavities can be used over an octave-spanning frequency range with adequate coatings. We also show directly that shape deviations caused by the fiber's index profile lead to a finesse decrease as observed in earlier attempts to build long FFP cavities, and show a way to overcome this problem

Implication des fonctions mitochondriales dans l'effet cardioprotecteur induit par la sur-expression de la protéine H11 kinase/Hsp22 chez la souris

Development of reperfusion strategies such as thrombolysis, angioplasty and cardiac surgery to restore blood flow after myocardial ischemia is responsible for a spectacular reduction in deleterious consequences resulting from acute coronary syndrome. However reperfusion itself causes supplementary lesions. Research for new complementary cardioprotective strategies is needed to reduce the impact of myocardial ischemia. The discovery of powerful intrinsic cardioprotective processes consisting in repeated short cycles of ischemia-reperfusion (IR) before the ischemic episode (ischemic preconditioning) or at the moment of the reperfusion (ischemic postconditioning) has allowed to analyze the mechanisms involved in IR lesions and highlighted a crucial role of mitochondria and more particularly of the increase in its membrane permeability via the opening of the mitochondrial permeability transition pore (mPTP). Dr C. Depré et al. (2001) demonstrated that the over-expression of Hsp22 protein coding gene which induced myocardial hypertrophy protected from myocardial infarction. The mechanism of this innovative cardioprotective strategy is not fully understood but Hsp22 promotes the activation of cellular survival pathways such as the NO synthase pathway which is also involved in ischemic preconditioning (Depré et al., 2006).The goal of the first part of our study was to evaluate the effects of Hsp22 on mitochondrial functions and the role of NO in these effects using a transgenic mouse model overexpressing Hsp22 in the heart. Our results showed that Hsp22 overexpression increases mitochondrial NO production which stimulated oxidative phosphorylation in basal state. This was accompanied by an increased in reactive oxygen species (ROS) production by mitochondrial respiratory chain complex I. This overexpression also reduced the maximal capability of complex I and III to produce ROS production and limited mPTP opening. After anoxia, Hsp22 overexpression increaseed oxidative phosphorylation inhibition by a NO-dependent mechanism and limited the burst of ROS production from the respiratory chain.. Thus, Hsp22 modulates mitochondrial functions and this could participate to its cardioprotective effect as these characteristics replicate those of ischemic preconditioning. In the next step, we confirmed that Hsp22 overexpression highly reduced infarct size in an in vivo model of IR and showed that this was associated with a better preservation of mitochondrial functions.As ROS are key mediators of preconditioning but also of myocardial hypertrophy and aging and Hsp22 stimulates mitochondrial ROS production, induces a myocardial hypertrophy and a cardioprotective effect replicating preconditioning, we explored the role of ROS in Hsp22-induced effects in the last part of the study. Our results showed that Hsp22 overexpression activated major cellular sources of ROS leading to myocardial oxidative stress. This was associated with an extensive reduction of lifespan and the appearance of aging markers in the myocardium of young transgenic mice. Antioxidant treatment reduced the overproduction of ROS induced by Hsp22, decreased myocardial hypertrophy and restored lifespan in Hsp22 overexpressing mice showing the role of ROS in these effects. Finally, the cardioprotective effect induced by Hsp22 was maintained in old mice and was not dependent of ROS production. In conclusion, long-lasting cardioprotective effect induced by Hsp22 is associated with a NO-dependent preservation of mitochondrial functions and an oxidative stress responsible for myocardial hypertrophy and reduced lifespan. Antioxidant treatment is able to inhibit deleterious consequences of Hsp22 overexpression without affecting its cardioprotective effect.La reperméabilisation par thrombolyse, angioplastie ou chirurgie cardiaque des artères coronaires au décours d’un épisode d’ischémie myocardique est à l’origine d’une réduction spectaculaire de la morbi-mortalité de l’insuffisance coronaire aiguë. Elle est cependant la cause de lésions supplémentaires. La recherche de nouvelles approches cardioprotectrices complémentaires des méthodes de reperfusion actuelles est donc indispensable pour réduire les conséquences de l’ischémie myocardique. La découverte de puissants mécanismes cardioprotecteurs endogènes qui consistent en de brefs épisodes d’ischémie-reperfusion (IR) réalisés avant l’ischémie (pré-conditionnement ischémique, PCI) ou lors de la reperfusion (post-conditionnement ischémique) a permis de déterminer les mécanismes intervenant dans l’établissement des lésions d’IR. Le rôle prépondérant de la mitochondrie et l’augmentation de la perméabilité de ses membranes notamment via l’ouverture du pore de transition de perméabilité mitochondriale (mPTP) a pu être mis en évidence.Depré et al. (2001) ont décrit une stratégie cardioprotectrice novatrice : la surexpression de la protéine Hsp22 chez la souris protège le myocarde de l’infarctus et induit l’hypertrophie de ce dernier. Cette protéine est en effet capable d’activer des acteurs clés de la survie cellulaire notamment la voie des NO synthases qui est fortement impliquée dans le processus de PCI.Dans un premier temps, nous avons étudié les effets d’Hsp22 sur les fonctions mitochondriales et analysé le rôle du NO dans ces effets à l’aide d’un modèle murin sur-exprimant Hsp22 dans le myocarde. Nous avons montré qu’à l’état basal, la sur-expression d’Hsp22 augmente la production mitochondriale de NO, ce qui stimule la phosphorylation oxydative et s’accompagne de l’augmentation de la production d’espèces réactives de l’oxygène (ERO) par le complexe I de la chaîne respiratoire mitochondriale. Cette sur-expression réduit également la capacité maximale des complexes I et III à produire des ERO et limite l’ouverture du mPTP. Après anoxie, la sur-expression d’ Hsp22 exacerbe la diminution de phosphorylation oxydative par un mécanisme dépendant du NO et réduit la surproduction d’ERO par la chaîne respiratoire. Ces caractéristiques sont semblables à celles conférées par le PCI. La protéine Hsp22 induit donc au niveau mitochondrial des modifications qui pourraient participer à son effet cardioprotecteur. Une étude sur un modèle d’IR in vivo a permis de confirmer qu’Hsp22 limite fortement la taille de l’infarctus et de montrer que cet effet est associé à une réduction de l’atteinte des fonctions mitochondriales après IR. Les ERO sont des médiateurs clés dans le PCI mais également dans le développement de l’hypertrophie myocardique et du vieillissement prématuré. Or, Hsp22 stimule la production d’ERO mitochondriales, induit une hypertrophie myocardique et un effet cardioprotecteur similaire au PCI. Nous avons donc étudié le rôle des ERO dans les effets induits par Hsp22. Nos résultats ont montré qu’Hsp22 active les principales sources d’ERO cellulaires dans le myocarde aboutissant à un stress oxydant. Cet effet est associé à une forte réduction de la durée de vie des animaux sur-exprimant Hsp22 et à l’apparition de marqueurs de vieillissement prématuré dans le myocarde. Un traitement antioxydant permet de réduire cette sur-production d’ERO ainsi que l’hypertrophie myocardique et de rétablir l’espérance de vie des animaux transgéniques. Enfin, l’effet cardioprotecteur induit par Hsp22 est maintenu avec l’âge et n’est pas dépendant des ERO.En conclusion, l’effet cardioprotecteur durable induit par Hsp22 est associé à une protection des fonctions mitochondriales NO dépendante mais s’accompagne d’un stress oxydant responsable de l’hypertrophie myocardique et de la réduction de la durée de vie. Un traitement antioxydant est capable d’inhiber les effets délétères induits pas Hsp22 sans affecter son effet cardioprotecteur

Enhanced and reduced atom number fluctuations in a BEC splitter

We measure atom number statistics after splitting a gas of ultracold 87Rb atoms in a purely magnetic double-well potential created on an atom chip. Well below the critical temperature for Bose-Einstein condensation T_c, we observe reduced fluctuations down to -4.9dB below the atom shot noise level. Fluctuations rise to more than +3.8dB close to T_c, before reaching the shot noise level for higher temperatures. We use two-mode and classical field simulations to model these results. This allows us to confirm that the super-shot noise fluctuations directly originate from quantum statistics

Mapping standing-wave cavity modes with a commercial scanning near-field microscope tip

We describe a method to map the standing-wave pattern inside a Fabry-Perot optical cavity with sub-wavelength resolution by perturbing it with a commercially available scanning near-field optical microscope (SNOM) tip. The method is applied to a fiber Fabry-Perot microcavity. We demonstrate its use to determine the relative position of the antinodes at two different wavelengths. In addition, we use the SNOM tip as a point-like source allowing precise positioning of a microscope objective with respect to the cavity mode

Cavity-based single atom preparation and high-fidelity hyperfine state readout

We prepare and detect the hyperfine state of a single 87Rb atom coupled to a fiber-based high finesse cavity on an atom chip. The atom is extracted from a Bose-Einstein condensate and trapped at the maximum of the cavity field, resulting in a reproducibly strong atom-cavity coupling. We use the cavity reflection and transmission signal to infer the atomic hyperfine state with a fidelity exceeding 99.92% in a read-out time of 100 microseconds. The atom is still trapped after detection.Comment: 5 pages, 4 figure