Optical manipulation of a single Mn spin in a CdTe-based quantum dot

A system of two coupled CdTe quantum dots, one of them containing a single Mn ion, was studied in continuous wave and modulated photoluminescence, photoluminescence excitation, and photon correlation experiments. Optical writing of information in the spin state of the Mn ion has been demonstrated, using orientation of the Mn spin by spin-polarized carriers transferred from the neighbor quantum dot. Mn spin orientation time values from 20 ns to 100 ns were measured, depending on the excitation power. Storage time of the information in the Mn spin was found to be enhanced by application of a static magnetic field of 1 T, reaching hundreds of microseconds in the dark. Simple rate equation models were found to describe correctly static and dynamical properties of the system.Comment: 4 pages, 3 figure

Single spin optical read-out in CdTe/ZnTe quantum dot studied by photon correlation spectroscopy

Spin dynamics of a single electron and an exciton confined in CdTe/ZnTe quantum dot is investigated by polarization-resolved correlation spectroscopy. Spin memory effects extending over at least a few tens of nanoseconds have been directly observed in magnetic field and described quantitatively in terms of a simple rate equation model. We demonstrate an effective (68%) all-optical read-out of the single carrier spin state through probing the degree of circular polarization of exciton emission after capture of an oppositely charged carrier. The perturbation introduced by the pulsed optical excitation serving to study the spin dynamics has been found to be the main source of the polarization loss in the read-out process. In the limit of low laser power the read-out efficiency extrapolates to a value close to 100%. The measurements allowed us as well to determine neutral exciton spin relaxation time ranging from 3.4 +/- 0.1 ns at B = 0 T to 16 +/- 3 ns at B = 5 T.Comment: to appear in Phys. Rev.

Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance

Autophagy is an ancient, intracellular degradative system which plays important roles in regulating protein homeostasis and which is essential for survival when cells are faced with metabolic stress. Increasing evidence suggests that autophagy also functions as a tumor suppressor mechanism that harnesses the growth and/or survival of cells as they transition towards a rapidly dividing malignant state. However, the impact of autophagy on cancer progression and on the efficacy of cancer therapeutics is controversial. In particular, although the induction of autophagy has been reported after treatment with a number of therapeutic agents, including imatinib, this response has variously been suggested to either impair or contribute to the effects of anticancer agents. More recent studies support the notion that autophagy compromises the efficacy of anticancer agents, where agents such as chloroquine (CQ) that impair autophagy augment the anticancer activity of histone deacetylase (HDAC) inhibitors and alkylating agents. Inhibition of autophagy is a particularly attractive strategy for the treatment of imatinib-refractory chronic myelogenous leukemia (CML) since a combination of CQ with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) compromises the survival of even BCR-ABL-T315I+ imatinib-resistant CML. Additional studies are clearly needed to establish the clinical utility of autophagy inhibitors and to identify patients most likely to benefit from this novel therapeutic approach