Spin and energy transfer in nanocrystals without transport of charge

We describe a mechanism of spin transfer between individual quantum dots that does not require tunneling. Incident circularly-polarized photons create inter-band excitons with non-zero electron spin in the first quantum dot. When the quantum-dot pair is properly designed, this excitation can be transferred to the neighboring dot via the Coulomb interaction with either {\it conservation} or {\it flipping} of the electron spin. The second dot can radiate circularly-polarized photons at lower energy. Selection rules for spin transfer are determined by the resonant conditions and by the strong spin-orbit interaction in the valence band of nanocrystals. Coulomb-induced energy and spin transfer in pairs and chains of dots can become very efficient under resonant conditions. The electron can preserve its spin orientation even in randomly-oriented nanocrystals.Comment: 13 pages, 3 figure

Increased sensitivity to radiochemotherapy in IDH1 mutant glioblastoma as demonstrated by serial quantitative MR volumetry

10.1093/neuonc/not198Neuro-Oncology163414-420NEUR

Novel Model of Frontal Impact Closed Head Injury in the Rat

Frontal impact, closed head trauma is a frequent cause of traumatic brain injury (TBI) in motor vehicle and sports accidents. Diffuse axonal injury (DAI) is common in humans and experimental animals, and results from shearing forces that develop within the anisotropic brain. Because the specific anisotropic properties of the brain are axis-dependent, the anatomical site where force is applied as well as the resultant acceleration, be it linear, rotational, or some combination, are important determinants of the resulting pattern of brain injury. Available rodent models of closed head injury do not reproduce the frontal impact commonly encountered in humans. Here we describe a new rat model of closed head injury that is a modification of the impact-acceleration model of Marmarou. In our model (the Maryland model), the impact force is applied to the anterior part of the cranium and produces TBI by causing anterior-posterior plus sagittal rotational acceleration of the brain inside the intact cranium. Skull fractures, prolonged apnea, and mortality were absent. The animals exhibited petechial hemorrhages, DAI marked by a bead-like pattern of β-amyloid precursor protein (β-APP) in damaged axons, and widespread upregulation of β-APP in neurons, with regions affected including the orbitofrontal cortex (coup), corpus callosum, caudate, putamen, thalamus, cerebellum, and brainstem. Activated caspase-3 was prominent in hippocampal neurons and Purkinje cells at the grey-white matter junction of the cerebellum. Neurobehavioral dysfunction, manifesting as reduced spontaneous exploration, lasted more than 1 week. We conclude that the Maryland model produces diffuse injuries that may be relevant to human brain injury