762 research outputs found

    Magneto-optics in pure and defective Ga_{1-x}Mn_xAs from first-principles

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    The magneto-optical properties of Ga1βˆ’x_{1-x}Mnx_{x}As including their most common defects were investigated with precise first--principles density-functional FLAPW calculations in order to: {\em i}) elucidate the origin of the features in the Kerr spectra in terms of the underlying electronic structure; {\em ii}) perform an accurate comparison with experiments; and {\em iii}) understand the role of the Mn concentration and occupied sites in shaping the spectra. In the substitutional case, our results show that most of the features have an interband origin and are only slightly affected by Drude--like contributions, even at low photon energies. While not strongly affected by the Mn concentration for the intermediately diluted range (x∼x\sim 10%), the Kerr factor shows a marked minimum (up to 1.5o^o) occurring at a photon energy of ∼\sim 0.5 eV. For interstitial Mn, the calculated results bear a striking resemblance to the experimental spectra, pointing to the comparison between simulated and experimental Kerr angles as a valid tool to distinguish different defects in the diluted magnetic semiconductors framework.Comment: 10 pages including 2 figures, submitted to Phys. Rev.

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    Calmodulin’s Interaction with Ξ±- Synuclein, a Protein Implicated in Parkinson’s Disease

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    60,000 people in one year diagnosed, 1 million in the United States, and over 10 million worldwide have Parkinson’s disease (PD), which is the 2nd most common neurodegenerative disease. PD is prevalent in males and is typically seen in patients in their 60s. The most notable symptom of PD is the degeneration of neuronal control, especially in the hands. Over 156millionisspentonresearchingthisdiseaseandabout156 million is spent on researching this disease and about 25 billion is spent for diagnosed patients each year. Aside from managing the financial burdens of PD, patients also have physical burdens. Most patients develop tremors and have difficulties writing, eating, and can degenerate quickly. The PD has previously been attributed to the lack of the neurotransmitter, dopamine, in the patient’s brain; however recent biochemical studies have surfaced other biomolecular mechanisms that attribute to PD, such as the interaction between Calmodulin and Ξ±-Synuclein. Calmodulin (CaM) is a protein found in the brain of healthy patients and is an intermediate calcium (Ca2+) binding messenger with over 100 different targets in eukaryotic cells. Ξ±- Synuclein (Ξ±-Syn) is a protein found at the ends of neurons in the presynaptic terminals in healthy patients, suggesting involvement with neurotransmitter signaling, however the exact function of Ξ±- Syn is still under investigation. Recent studies show that Ξ±- Syn and CaM interact resulting in protein aggregation. The Ξ±- Syn aggregation is the main structural component of Lewy bodies which is enhanced in the presence of Ca2+. Lewy bodies are known to develop in cranial nerve cells of PD patients and interrupts neuronal function. Little is known about how Lewy bodies attribute to abnormalities in PD patients, but there are connections to low levels of acetylcholine and dopamine, in addition to an interruption of signals between nerve cells. By using fluorescence spectroscopy, we studied the interaction between Ξ±- Syn and CaM and explore Ca2+’s role in the interaction that promotes the degenerateness of PD patients

    Multimode Memories in Atomic Ensembles

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    The ability to store multiple optical modes in a quantum memory allows for increased efficiency of quantum communication and computation. Here we compute the multimode capacity of a variety of quantum memory protocols based on light storage in ensembles of atoms. We find that adding a controlled inhomogeneous broadening improves this capacity significantly.Comment: Published version. Many thanks are due to Christoph Simon for his help and suggestions. (This acknowledgement is missing from the final draft: apologies!

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    ВСория эффСкта Π°ΠΌΠ°Π»ΡŒΠ³Π°ΠΌΡ‹ аммония Π² ΠΌΠ΅Ρ‚ΠΎΠ΄Π΅ АПН

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    Efficient spatially-resolved multimode quantum memory

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    We propose a method that enables efficient storage and retrieval of a photonic excitation stored in an ensemble quantum memory consisting of Lambda-type absorbers with non-zero Stokes shift. We show that this can be used to implement a multimode quantum memory storing multiple frequency-encoded qubits in a single ensemble, and allowing their selective retrieval. The read-out scheme applies to memory setups based on both electromagnetically-induced transparency and stimulated Raman scattering, and spatially separates the output signal field from the control fields

    Total arrest of spontaneous and evoked synaptic transmission but normal synaptogenesis in the absence of Munc13-mediated vesicle priming

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    Synaptic vesicles must be primed to fusion competence before they can fuse with the plasma membrane in response to increased intracellular Ca2+ levels. The presynaptic active zone protein Munc13-1 is essential for priming of glutamatergic synaptic vesicles in hippocampal neurons. However, a small subpopulation of synapses in any given glutamatergic nerve cell as well as all gamma-aminobutyratergic (GABAergic) synapses are largely independent of Munc13-1. We show here that Munc13-2, the only Muncl 3 isoform coexpressed with Munc13-1 in hippocampus, is responsible for vesicle priming in Munc13-1 independent hippocampal synapses. Neurons lacking both Munc13-1 and Munc13- 2 show neither evoked nor spontaneous release events, yet form normal numbers of synapses with typical ultrastructural features. Thus, the two Munc13 isoforms are completely redundant in GABAergic cells whereas glutamatergic neurons form two types of synapses, one of which is solely Munc13-1 dependent and lacks Munc13-2 whereas the other type employs Munc13-2 as priming factor. We conclude that Munc13-mediated vesicle priming is not a transmitter specific phenomenon but rather a general and essential feature of multiple fast neurotransmitter systems, and that synaptogenesis during development is not dependent on synaptic secretory activity
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