Ultrafast light-induced magnetization dynamics in ferromagnetic semiconductors

We develop a theory of the magnetization dynamics triggered by ultrafast optical excitation of ferromagnetic semiconductors. We describe the effects of the strong carrier spin relaxation on the nonlinear optical response by using the Lindblad semigroup method. We demonstrate magnetization control during femtosecond timescales via the interplay between circularly polarized optical excitation, hole-spin damping, polarization dephasing, and the Mn-hole spin interactions. Our results show a light-induced magnetization precession and relaxation for the duration of the optical pulse.Comment: 4 pages, 2 figure

Signatures of spin blockade in the optical response of a charged quantum dot

We model spin blockade for optically excited electrons and holes in a charged semiconductor quantum dot. We study the case where the quantum dot is initially charged with a single electron and is then filled with an additional, optically excited electron-hole pair, thus forming a charged exciton (trion). To make contact with recent experiments, we model an optical pump-probe setup, in which the two lowest quantum dot levels (s and p shells) are photo excited. Using the Lindblad master equation, we calculate the differential transmission spectrum as a function of the pump-probe time delay. Taking into account both spin conserving and spin-flip intraband relaxation processes, we find that the presence of the ground-state electron spin leads to an optical spin blockade at short delay times which is visible as a crossover between two exponential decays of the differential transmission. To make predictions for future experiments, we also study the dependence of the spin-blockade on an external magnetic field.Comment: 8 pages, 8 figure

Strong Electronic Correlation Effects in Coherent Multidimensional Nonlinear Optical Spectroscopy

We discuss a many−body theory of the coherent ultrafast nonlinear optical response of systems with a strongly correlated electronic ground state that responds unadiabatically to photoexcitation. We introduce a truncation of quantum kinetic density matrix equations of motion that does not rely on an expansion in terms of the interactions and thus applies to strongly correlated systems. For this we expand in terms of the optical field, separate out contributions to the time−evolved many−body state due to correlated and uncorrelated multiple optical transitions, and use “Hubbard operator” density matrices to describe the exact dynamics of the individual contributions within a subspace of strongly coupled states, including “pure dephasing”. Our purpose is to develop a quantum mechanical tool capable of exploring how, by coherently photoexciting selected modes, one can trigger nonlinear dynamics of strongly coupled degrees of freedom. Such dynamics could lead to photoinduced phase transitions. We apply our theory to the nonlinear response of a two−dimensional electron gas (2DEG) in a magnetic field. We coherently photoexcite the two lowest Landau level (LL) excitations using three time−delayed optical pulses. We identify some striking temporal and spectral features due to dynamical coupling of the two LLs facilitated by inter−Landau−level magnetoplasmon and magnetoroton excitations and compare to three−pulse four−wave−mixing (FWM) experiments. We show that these features depend sensitively on the dynamics of four−particle correlations between an electron−hole pair and a magnetoplasmon/magnetoroton, reminiscent of exciton−exciton correlations in undoped semiconductors. Our results shed light into unexplored coherent dynamics and relaxation of the quantum Hall system (QHS) and can provide new insight into non−equilibrium co−operative phenomena in strongly correlated systems

Observation of inter-Landau-level quantum coherence in semiconductor quantum wells

Using three-pulse four-wave-mixing femtosecond spectroscopy, we excite a non-radiative coherence between the discrete Landau levels of an undoped quantum well and study its dynamics. We observe quantum beats that reflect the time evolution of the coherence between the two lowest Landau level magnetoexcitons. We interpret our observations using a many-body theory and find that the inter Landau level coherence decays with a new time constant, substantially longer than the corresponding interband magnetoexciton dephasing times. Our results indicate a new intraband excitation dynamics that cannot be described in terms of uncorrelated interband excitations.Comment: 5 pages, 5 figures, to appear in Phys. Rev. B Rapid Communication

Ultrafast dynamics of coherences in the quantum Hall system

Using three-pulse four-wave-mixing optical spectroscopy, we study the ultrafast dynamics of the quantum Hall system. We observe striking differences as compared to an undoped system, where the 2D electron gas is absent. In particular, we observe a large off-resonant signal with strong oscillations. Using a microscopic theory, we show that these are due to many-particle coherences created by interactions between photoexcited carriers and collective excitations of the 2D electron gas. We extract quantitative information about the dephasing and interference of these coherences.Comment: 4 pages, 4 figures, to be published in Phys. Rev. Let

Tyrosine kinase Flt3/Flt3-ligand signaling in the modulation of immune responses in experimental arthritis

Rheumatoid arthritis (RA) is an autoimmune, chronic systemic inflammatory disorder that primarily affects flexible joints resulting in severe joint destruction and disability if left untreated. Today, advances in treatment have significantly improved the outcome for patients, although the pathogenesis of RA remains relatively unknown. Signaling through the tyrosine kinase receptor fms-like tyrosine kinase 3 (Flt3) has been suggested to play a part in the RA pathogenesis. Flt3 is primarily expressed on hematopoietic stem cells and lymphoid progenitors in the bone marrow and has an important role in early B-cell development and formation of dendritic cells (DC). Furthermore, the ligand for Flt3 (Flt3L) serves as a regulator of regulatory T-cell (Treg) homeostasis and has been suggested to support differentiation of bone-resorbing osteoclasts. This thesis aimed to investigate the effect of Flt3/Flt3L signaling on the immune system during development of arthritis using an experimental animal model of human RA. Our study shows that Flt3 signaling supports formation of DCs and Treg cells during arthritis development. Treg expansion associated with Flt3L treatment resulted in a reduced production of inflammatory cytokines, reduced levels of antigen-specific antibodies and reduced bone destruction. On the contrary, lack of Flt3L was associated with reduced Treg formation resulting in loss of control over T-cell proliferation, and bone destruction during arthritis. Flt3L was found to positively influence the transcription of the osteoclast-regulating factor IRF8, and could by this mechanism influence osteoclast formation. Impaired signaling through Flt3 resulted in low IRF8 expression, accumulation of osteoclasts in the arthritic joint and an increased loss of femoral trabecular bone. Conversely, Flt3L treatment was associated with increased IRF8 expression, reduced osteoclast formation and restoration of trabecular bone formation in mice lacking Flt3L (Flt3LKO). Finally, we could identify a previously unacknowledged role for Flt3 in peripheral B-cell responses. We demonstrated that Flt3 was re-expressed on activated B-cells following LPS stimulation in vitro and on a population of germinal center B-cells in vivo. By using Flt3LKO mice we could identify an important role for Flt3L in class switch recombination (CSR) to IgG1. B-cells from Flt3LKO mice were found have reduced activation of Stat6 after IL-4 stimulation, resulting in impaired initiation of CSR to IgG1 and highly reduced formation of IgG1+ B-cells and IgG1 production. In summary this thesis shows that Flt3L has an important function in regulating DC and Treg homeostasis and function during arthritis. Furthermore, Flt3L has a regulatory role on osteoclast development and on trabecular bone formation. Finally, signaling through the Flt3 receptor on activated B-cells has an important role in the CSR process and deficiency of Flt3L leads to a skewed antibody response towards the more potent IgG subclasses IgG2b and IgG2c. Together, these results suggest that Flt3L might play a protective role during arthritis by reduction of bone destruction, induction of regulatory T-cells and regulation of antibody effector functions. The conclusion of this thesis is that signaling through the tyrosine kinase Flt3 plays an important role in modulating immune responses during experimental arthritis