Cooperativity in light scattering by cold atoms

A cloud of cold N two-level atoms driven by a resonant laser beam shows cooperative effects both in the scattered radiation field and in the radiation pressure force acting on the cloud center-of-mass. The induced dipoles synchronize and the scattered light presents superradiant and/or subradiant features. We present a quantum description of the process in terms of a master equation for the atomic density matrix in the scalar, Born-Markov approximations, reduced to the single-excitation limit. From a perturbative approach for weak incident field, we derive from the master equation the effective Hamiltonian, valid in the linear regime. We discuss the validity of the driven timed Dicke ansatz and of a partial wave expansion for different optical thicknesses and we give analytical expressions for the scattered intensity and the radiation pressure force on the center of mass. We also derive an expression for collective suppression of the atomic excitation and the scattered light by these correlated dipoles.Comment: 15 pages, 8 figure

Fast compression of a cold atomic cloud using a blue detuned crossed dipole trap

We present the experimental realization of a compressible blue detuned crossed dipole trap for cold atoms allowing for fast dynamical compression (~ 5 - 10 ms) of 5x10^7 Rubidium atoms up to densities of ~ 10^13 cm^-3. The dipole trap consists of two intersecting tubes of blue-detuned laser light. These tubes are formed using a single, rapidly rotating laser beam which, for sufficiently fast rotation frequencies, can be accurately described by a quasi-static potential. The atomic cloud is compressed by dynamically reducing the trap volume leading to densities close to the Ioffe-Reggel criterion for light localization.Comment: 14 pages, 15 figures, 2 table

Interplay between radiation pressure force and scattered light intensity in the cooperative scattering by cold atoms

The interplay between the superradiant emission of a cloud of cold two-level atoms and the radiation pressure force is discussed. Using a microscopic model of coupled atomic dipoles driven by an external laser, the radiation field and the average radiation pressure force are derived. A relation between the far-field scattered intensity and the force is derived, using the optical theorem. Finally, the scaling of the sample scattering cross section with the parameters of the system is studied.Comment: 10 pages, 3 figures, article for special issue of PQE 201

Atom and photon measurement in cooperative scattering by cold atoms

In this paper, we study cooperative scattering of low intensity light by a cloud of N two-level systems. We include the incident laser field driving these two-level systems and compute the radiation pressure force on the center of mass of the cloud. This signature is of particular interest for experiments with laser cooled atoms. Including the complex coupling between dipoles in a scalar model for dilute clouds of two-level systems, we obtain expression for cooperative scattering forces taking into account the collective Lamb shift. We also derive the expression of the radiation pressure force on a large cloud of two-level systems from an heuristic approach and show that at lowest driving intensities this force is identical for a product and an entangled state.Comment: 11 pages, 4 figures, article for special issue of PQE 201

Cooperative Scattering by Cold Atoms

We have studied the interplay between disorder and cooperative scattering for single scattering limit in the presence of a driving laser. Analytical results have been derived and we have observed cooperative scattering effects in a variety of experiments, ranging from thermal atoms in an optical dipole trap, atoms released from a dark MOT and atoms in a BEC, consistent with our theoretical predictions.Comment: submitted for special issue of PQE 201

Interplay of superradiance and disorder in the Anderson Model

Using a non-Hermitian Hamiltonian approach to open systems, we study the interplay of disorder and superradiance in a one-dimensional Anderson model. Analyzing the complex eigenvalues of the non-Hermitian Hamiltonian, a transition to a superradiant regime is shown to occur. As an effect of openness the structure of eigenstates undergoes a strong change in the superradiant regime: we show that the sensitivity to disorder of the superradiant and the subradiant subspaces is very different; superradiant states remain delocalized as disorder increases, while subradiant states are sensitive to the degree of disorder.Comment: 7 pages, submitted to the special issue on "Physics with non-Hermitian operators: Theory and Experiment" of the journal "Fortschritte der Physik - Progress of Physics

Mutations in components of complement influence the outcome of Factor I-associated atypical hemolytic uremic syndrome

Genetic studies have shown that mutations of complement inhibitors such as membrane cofactor protein, Factors H, I, or B and C3 predispose patients to atypical hemolytic uremic syndrome (aHUS). Factor I is a circulating serine protease that inhibits complement by degrading C3b and up to now only a few mutations in the CFI gene have been characterized. In a large cohort of 202 patients with aHUS, we identified 23 patients carrying exonic mutations in CFI. Their overall clinical outcome was unfavorable, as half died or developed end-stage renal disease after their first syndrome episode. Eight patients with CFI mutations carried at least one additional known genetic risk factor for aHUS, such as a mutation in MCP, CFH, C3 or CFB; a compound heterozygous second mutation in CFI; or mutations in both the MCP and CFH genes. Five patients exhibited homozygous deletion of the Factor H-related protein 1 (CFHR-1) gene. Ten patients with aHUS had one mutation in their CFI gene (Factor I-aHUS), resulting in a quantitative or functional Factor I deficiency. Patients with a complete deletion of the CFHR-1 gene had a significantly higher risk of a bad prognosis compared with those with one Factor I mutation as their unique vulnerability feature. Our results emphasize the necessity of genetic screening for all susceptibility factors in patients with aHUS

Actualización en síndrome hemolítico urémico atípico: diagnóstico y tratamiento. Documento de consenso. Revisión

Podeu consultar la versió en castellà del document a: http://dx.doi.org/10.1016/j.nefro.2015.07.005Haemolytic uraemic syndrome (HUS) is a clinical entity defined as the triad of nonimmune haemolytic anaemia, thrombocytopenia, and acute renal failure, in which the underlying lesions are mediated by systemic thrombotic microangiopathy (TMA). Different causes can induce the TMA process that characterises HUS. In this document we consider atypical HUS (aHUS) a sub-type of HUS in which the TMA phenomena are the consequence of the endotelial damage in the microvasculature of the kidneys and other organs due to a disregulation of the activity of the complement system. In recent years, a variety of aHUs-related mutations have been identified in genes of the complement system, which can explain approximately 60% of the aHUS cases, and a number of mutations and polymorphisms have been functionally characterised. These findings have stablished that aHUS is a consequence of the insufficient regulation of the activation of the complement on cell surfaces, leading to endotelial damage mediated by C5 and the complement terminal pathway. Eculizumab is a monoclonal antibody that inhibits the activation of C5 and blocks the generation of the pro-inflammatory molecule C5a and the formation of the cell membrane attack complex. In prospective studies in patients with aHUS, the use of Eculizumab has shown a fast and sustained interruption of the TMA process and it has been associated with significative long-term improvements in renal function, the interruption of plasma therapy and important reductions in the need of dialysis. According to the existing literature and the accumulated clinical experience, the Spanish aHUS Group published a consensus document with recommendations for the treatment of aHUs (Nefrologia 2013;33[1]:27-45). In the current online version of this document, we update the aetiological classification of TMAs, the pathophysiology of aHUS, its differential diagnosis and its therapeutic management

aHUS caused by complement dysregulation: new therapies on the horizon

Atypical hemolytic uremic syndrome (aHUS) is a heterogeneous disease that is caused by defective complement regulation in over 50% of cases. Mutations have been identified in genes encoding both complement regulators [complement factor H (CFH), complement factor I (CFI), complement factor H-related proteins (CFHR), and membrane cofactor protein (MCP)], as well as complement activators [complement factor B (CFB) and C3]. More recently, mutations have also been identified in thrombomodulin (THBD), an anticoagulant glycoprotein that plays a role in the inactivation of C3a and C5a. Inhibitory autoantibodies to CFH account for an additional 5–10% of cases and can occur in isolation or in association with mutations in CFH, CFI, CFHR 1, 3, 4, and MCP. Plasma therapies are considered the mainstay of therapy in aHUS secondary to defective complement regulation and may be administered as plasma infusions or plasma exchange. However, in certain cases, despite initiation of plasma therapy, renal function continues to deteriorate with progression to end-stage renal disease and renal transplantation. Recently, eculizumab, a humanized monoclonal antibody against C5, has been described as an effective therapeutic strategy in the management of refractory aHUS that has failed to respond to plasma therapy. Clinical trials are now underway to further evaluate the efficacy of eculizumab in the management of both plasma-sensitive and plasma-resistant aHUS

Genetics and complement in atypical HUS

Central to the pathogenesis of atypical hemolytic uremic syndrome (aHUS) is over-activation of the alternative pathway of complement. Following the initial discovery of mutations in the complement regulatory protein, factor H, mutations have been described in factor I, membrane cofactor protein and thrombomodulin, which also result in decreased complement regulation. Autoantibodies to factor H have also been reported to impair complement regulation in aHUS. More recently, gain of function mutations in the complement components C3 and Factor B have been seen. This review focuses on the genetic causes of aHUS, their functional consequences, and clinical effect