Stability of negative and positive trions in quantum wires

Binding energies of negative ($X^-$) and positive trions ($X^+$) in quantum wires are studied for strong quantum confinement of carriers which results in a numerical exactly solvable model. The relative electron and hole localization has a strong effect on the stability of trions. For equal hole and electron confinement, $X^+$ is more stable but a small imbalance of the particle localization towards a stronger hole localization e.g. due to its larger effective mass, leads to the interchange of $X^-$ and $X^+$ recombination lines in the photoluminescent spectrum as was recently observed experimentally. In case of larger $X^-$ stability, a magnetic field oriented parallel to the wire axis leads to a stronger increase of the $X^+$ binding energy resulting in a crossing of the $X^+$ and $X^-$ lines

Exciton and negative trion dissociation by an external electric field in vertically coupled quantum dots

We study the Stark effect for an exciton confined in a pair of vertically coupled quantum dots. A single-band approximation for the hole and a parabolic lateral confinement potential are adopted which allows for the separation of the lateral center-of-mass motion and consequently for an exact numerical solution of the Schr\"odinger equation. We show that for intermediate tunnel coupling the external electric field leads to the dissociation of the exciton via an avoided crossing of bright and dark exciton energy levels which results in an atypical form of the Stark shift. The electric-field-induced dissociation of the negative trion is studied using the approximation of frozen lateral degrees of freedom. It is shown that in a symmetric system of coupled dots the trion is more stable against dissociation than the exciton. For an asymmetric system of coupled dots the trion dissociation is accompanied by a positive curvature of the recombination energy line as a function of the electric field.Comment: PRB - in prin

In situ biospectroscopic investigation of rapid ischemic and postmortem induced biochemical alterations in the rat brain

© 2014 American Chemical Society. Rapid advances in imaging technologies have pushed novel spectroscopic modalities such as Fourier transform infrared spectroscopy (FTIR) and X-ray absorption spectroscopy (XAS) at the sulfur K-edge to the forefront of direct in situ investigation of brain biochemistry. However, few studies have examined the extent to which sample preparation artifacts confound results. Previous investigations using traditional analyses, such as tissue dissection, homogenization, and biochemical assay, conducted extensive research to identify biochemical alterations that occur ex vivo during sample preparation. In particular, altered metabolism and oxidative stress may be caused by animal death. These processes were a concern for studies using biochemical assays, and protocols were developed to minimize their occurrence. In this investigation, a similar approach was taken to identify the biochemical alterations that are detectable by two in situ spectroscopic methods (FTIR, XAS) that occur as a consequence of ischemic conditions created during humane animal killing. FTIR and XAS are well suited to study markers of altered metabolism such as lactate and creatine (FTIR) and markers of oxidative stress such as aggregated proteins (FTIR) and altered thiol redox (XAS). The results are in accordance with previous investigations using biochemical assays and demonstrate that the time between animal death and tissue dissection results in ischemic conditions that alter brain metabolism and initiate oxidative stress. Therefore, future in situ biospectroscopic investigations utilizing FTIR and XAS must take into consideration that brain tissue dissected from a healthy animal does not truly reflect the in vivo condition, but rather reflects a state of mild ischemia. If studies require the levels of metabolites (lactate, creatine) and markers of oxidative stress (thiol redox) to be preserved as close as possible to the in vivo condition, then rapid freezing of brain tissue via decapitation into liquid nitrogen, followed by chiseling the brain out at dry ice temperatures is required

Mapping alterations to the endogenous elemental distribution within the lateral ventricles and choroid plexus in brain disorders using X-ray fluorescence imaging

The choroid plexus and cerebral ventricles are critical structures for the production of cerebral spinal fluid (CSF) and play an important role in regulating ion and metal transport in the brain, however many aspects of its roles in normal physiology and disease states, such as psychiatric illness, remain unknown. The choroid plexus is difficult to examine in vivo, and in situ ex vivo, and as such has typically been examined indirectly with radiolabeled tracers or ex vivo stains, making measurements of the endogenous K+, Cl-, and Ca+ distributions unreliable. In the present study, we directly examined the distribution of endogenous ions and biologically relevant transition metals in the choroid plexus and regions surrounding the ventricles (ventricle wall, cortex, corpus callosum, striatum) using X-ray fluorescence imaging (XFI). We find that the choroid plexus was rich in Cl- and Fe while K+ levels increase further from the ventricle as Cl- levels decrease, consistent with the known role of ion transporters in the choroid plexus CSF production. A polyI:C offspring displayed enlarged ventricles, elevated Cl- surrounding the ventricles, and intraventricular calcifications. These observations fit with clinical findings in patients with schizophrenia and suggest maternal treatment with polyI:C may lead to dysfunctional ion regulation in offspring. This study demonstrates the power of XFI for examining the endogenous elemental distributions of the ventricular system in healthy brain tissue as well as disease models

X-ray fluorescence analysis of long-term changes in the levels and distributions of trace elements in the rat brain following mechanical injury

This paper describes the results of the application of X-ray fluorescence microscopy to the qualitative, topographic and quantitative elemental analysis of nervous tissue from rats with neocortical brain injury. The tissue samples were analyzed with a 15 μm beam defined by the size of the polycapillary focus. Raster scanning of the samples generated 2D cartographies, revealing the distributions of elements such as P, S, Cl, K, Ca, Fe, Cu, and Zn. Special emphasis was placed on the analysis of the areas neighboring the lesion site and the hippocampal formation tissue. The results obtained for rats with mechanical brain injuries were compared with those recorded for controls and animals with pilocarpine-induced seizures. There were no significant differences in the elemental compositions of gray and white matter between injured and uninjured brain hemispheres. A higher level of Ca was observed in the gray matter of both of the hemispheres in brains with neocortical injuries. A similar relation was noticed for Fe in the white matter. A comparative study of hippocampal formation tissue showed a statistically significant decrease in the mass per unit area of P in the dentate gyrus (DG) and the hilus (H) of DG for animals with brain lesions in comparison with the control group. Analogous relations were found for Cu in the DG and Zn in sector 3 of Ammon’s horn (CA3) and the DG. It is important to note that identical changes in the same areas were observed for animals with pilocarpine-induced seizures in our previous study

Synchrotron Radiation X-Ray Microfluorescence Reveals Polarized Distribution of Atomic Elements during Differentiation of Pluripotent Stem Cells

The mechanisms underlying pluripotency and differentiation in embryonic and reprogrammed stem cells are unclear. In this work, we characterized the pluripotent state towards neural differentiated state through analysis of trace elements distribution using the Synchrotron Radiation X-ray Fluorescence Spectroscopy. Naive and neural-stimulated embryoid bodies (EB) derived from embryonic and induced pluripotent stem (ES and iPS) cells were irradiated with a spatial resolution of 20 µm to make elemental maps and qualitative chemical analyses. Results show that these embryo-like aggregates exhibit self-organization at the atomic level. Metallic elements content rises and consistent elemental polarization pattern of P and S in both mouse and human pluripotent stem cells were observed, indicating that neural differentiation and elemental polarization are strongly correlated

Copper-Triggered Aggregation of Ubiquitin

Neurodegenerative disorders share common features comprising aggregation of misfolded proteins, failure of the ubiquitin-proteasome system, and increased levels of metal ions in the brain. Protein aggregates within affected cells often contain ubiquitin, however no report has focused on the aggregation propensity of this protein. Recently it was shown that copper, differently from zinc, nickel, aluminum, or cadmium, compromises ubiquitin stability and binds to the N-terminus with 0.1 micromolar affinity. This paper addresses the role of copper upon ubiquitin aggregation. In water, incubation with Cu(II) leads to formation of spherical particles that can progress from dimers to larger conglomerates. These spherical oligomers are SDS-resistant and are destroyed upon Cu(II) chelation or reduction to Cu(I). In water/trifluoroethanol (80∶20, v/v), a mimic of the local decrease in dielectric constant experienced in proximity to a membrane surface, ubiquitin incubation with Cu(II) causes time-dependent changes in circular dichroism and Fourier-transform infrared spectra, indicative of increasing β-sheet content. Analysis by atomic force and transmission electron microscopy reveals, in the given order, formation of spherical particles consistent with the size of early oligomers detected by gel electrophoresis, clustering of these particles in straight and curved chains, formation of ring structures, growth of trigonal branches from the rings, coalescence of the trigonal branched structures in a network. Notably, none of these ubiquitin aggregates was positive to tests for amyloid and Cu(II) chelation or reduction produced aggregate disassembly. The early formed Cu(II)-stabilized spherical oligomers, when reconstituted in 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) liposomes and in POPC planar bilayers, form annular and pore-like structures, respectively, which are common to several neurodegenerative disorders including Parkinson's, Alzheimer's, amyotrophic lateral sclerosis, and prion diseases, and have been proposed to be the primary toxic species. Susceptibility to aggregation of ubiquitin, as it emerges from the present study, may represent a potential risk factor for disease onset or progression while cells attempt to tag and process toxic substrates