Asymmetric Phosphorus Incorporation in Homoepitaxial P-Doped (111) Diamond Revealed by Photoelectron Holography

Diamond has two crystallographically inequivalent sites in the unit cell. In doped diamond, dopant occupation in the two sites is expected to be equal. Nevertheless, preferential dopant occupation during growth under nonequilibrium conditions is of fundamental importance, for example, to enhance the properties of nitrogen-vacancy (N-V) centers; therefore, this is a promising candidate for a qubit. However, the lack of suitable experimental techniques has made it difficult to study the crystal- and chemical-site-resolved local structures of dopants. Here, we confirm the identity of two chemical sites with asymmetric dopant incorporation in the diamond structure, via the photoelectron holography (PEH) of heavily phosphorus (P)-doped diamond prepared by chemical vapor deposition. One is substitutionally incorporated P with preferential site occupations and the other can be attributed to a PV split vacancy complex with preferential orientation. The present study shows that PEH is a valuable technique to study the local structures around dopants with a resolution of crystallographically inequivalent but energetically equivalent sites/orientations. Such information provides strategies to improve the properties of dopant related-complexes in which alignment is crucial for sensing of magnetic field or quantum spin register using N-V centers in diamond

Insights into GABA receptor signalling in TM3 Leydig cells

gamma-Aminobutyric acid (GABA) is an emerging signalling molecule in endocrine organs, since it is produced by endocrine cells and acts via GABA(A) receptors in a paracrine/autocrine fashion. Testicular Leydig cells are producers and targets for GABA. These cells express GABA(A) receptor subunits and in the murine Leydig cell line TM3 pharmacological activation leads to increased proliferation. The signalling pathway of GABA in these cells is not known in this study. We therefore attempted to elucidate details of GABA(A) signalling in TM3 and adult mouse Leydig cells using several experimental approaches. TM3 cells not only express GABA(A) receptor subunits, but also bind the GABA agonist {[}H-3] muscimol with a binding affinity in the range reported for other endocrine cells (K-d = 2.740 +/- 0.721 nM). However, they exhibit a low B-max value of 28.08 fmol/mg protein. Typical GABA(A) receptor-associated events, including Cl- currents, changes in resting membrane potential, intracellular Ca2+ or cAMP, were not measurable with the methods employed in TM3 cells, or, as studied in part, in primary mouse Leydig cells. GABA or GABA(A) agonist isoguvacine treatment resulted in increased or decreased levels of several mRNAs, including transcription factors (c-fos, hsf-1, egr-1) and cell cycle-associated genes (Cdk2, cyclin D1). In an attempt to verify the cDNA array results and because egr-1 was recently implied in Leydig cell development, we further studied this factor. RT-PCR and Western blotting confirmed a time-dependent regulation of egr-1 in TM3. In the postnatal testis egr-1 was seen in cytoplasmic and nuclear locations of developing Leydig cells, which bear GABA(A) receptors and correspond well to TM3 cells. Thus, GABA acts via an untypical novel signalling pathway in TM3 cells. Further details of this pathway remain to be elucidated. Copyright (c) 2005 S. Karger AG, Base

Origins of thermal spin depolarization in half-metallic ferromagnet CrO2_2

Using high-resolution spin-resolved photoemission spectroscopy, we observed a thermal spin depolarization to which all spin-polarized electrons contribute. Furthermore we observed a distinct minority spin state near the Fermi level and a corresponding depolarization that seldom contributes to demagnetization. The origin of this depolarization has been identified as the many-body effect characteristics of half-metallic ferromagnets. Our investigation opens an experimental field of itinerant ferromagnetic physics focusing on phenomena with sub-meV energy scale.Comment: 19 pages, 10 figure

Evolution of the remnant Fermi-surface state in the lightly doped correlated spin-orbit insulator Sr2-xLaxIrO4

The electronic structure of the lightly electron-doped correlated spin-orbit insulator Sr2IrO4 has been studied by angle-resolved photoelectron spectroscopy. We have observed the coexistence of a lower Hubbard band and an in-gap band; the momentum dependence of the latter traces that of the band calculations without on-site Coulomb repulsion. The in-gap state remained anisotropically gapped in all observed momentum areas, forming a remnant Fermi-surface state, evolving towards the Fermi energy by carrier doping. These experimental results show a striking similarity with those observed in deeply underdoped cuprates, suggesting the common nature of the nodal liquid states observed in both compounds

A Mechanism for the Polarity Formation of Chemoreceptors at the Growth Cone Membrane for Gradient Amplification during Directional Sensing

Accurate response to external directional signals is essential for many physiological functions such as chemotaxis or axonal guidance. It relies on the detection and amplification of gradients of chemical cues, which, in eukaryotic cells, involves the asymmetric relocalization of signaling molecules. How molecular events coordinate to induce a polarity at the cell level remains however poorly understood, particularly for nerve chemotaxis. Here, we propose a model, inspired by single-molecule experiments, for the membrane dynamics of GABA chemoreceptors in nerve growth cones (GCs) during directional sensing. In our model, transient interactions between the receptors and the microtubules, coupled to GABA-induced signaling, provide a positive-feedback loop that leads to redistribution of the receptors towards the gradient source. Using numerical simulations with parameters derived from experiments, we find that the kinetics of polarization and the steady-state polarized distribution of GABA receptors are in remarkable agreement with experimental observations. Furthermore, we make predictions on the properties of the GC seen as a sensing, amplification and filtering module. In particular, the growth cone acts as a low-pass filter with a time constant ∼10 minutes determined by the Brownian diffusion of chemoreceptors in the membrane. This filtering makes the gradient amplification resistent to rapid fluctuations of the external signals, a beneficial feature to enhance the accuracy of neuronal wiring. Since the model is based on minimal assumptions on the receptor/cytoskeleton interactions, its validity extends to polarity formation beyond the case of GABA gradient sensing. Altogether, it constitutes an original positive-feedback mechanism by which cells can dynamically adapt their internal organization to external signals

Self-tolerance in multiple sclerosis

During the last decade, several defects in self-tolerance have been identified in multiple sclerosis. Dysfunction in central tolerance leads to the thymic output of antigen-specific T cells with T cell receptor alterations favouring autoimmune reactions. In addition, premature thymic involution results in a reduced export of naïve regulatory T cells, the fully suppressive clone. Alterations in peripheral tolerance concern costimulatory molecules as well as transcriptional and epigenetic mechanisms. Recent data underline the key role of regulatory T cells that suppress Th1 and Th17 effector cell responses and whose immunosuppressive activity is impaired in patients with multiple sclerosis. Those recent observations suggest that a defect in self-tolerance homeostasis might be the primary mover of multiple sclerosis leading to subsequent immune attacks, inflammation and neurodegeneration. The concept of multiple sclerosis as a consequence of the failure of central and peripheral tolerance mechanisms to maintain a self-tolerance state, particularly of regulatory T cells, may have therapeutic implications. Restoring normal thymic output and suppressive functions of regulatory T cells appears an appealing approach. Regulatory T cells suppress the general local immune response via bystander effects rather than through individual antigen-specific responses. Interestingly, the beneficial effects of currently approved immunomodulators (interferons β and glatiramer acetate) are associated with a restored regulatory T cell homeostasis. However, the feedback regulation between Th1 and Th17 effector cells and regulatory T cells is not so simple and tolerogenic mechanisms also involve other regulatory cells such as B cells, dendritic cells and CD56bright natural killer cells