Two-center resonant photoionization-excitation driven by combined intra- and interatomic electron correlations

Ionization-excitation of an atom induced by the absorption of a single photon in the presence of a neighbouring atom is studied. The latter is, first, resonantly photoexcited and, afterwards, transfers the excitation energy radiationlessly to the other atom, leading to its ionization with simultaneous excitation. The process relies on the combined effects of interatomic and intraatomic electron correlations. Under suitable conditions, it can dominate by several orders of magnitude over direct photoionization-excitation and even over direct photoionization. In addition, we briefly discuss another kind of two-center resonant photoionization with excitation where the ionization and residual excitation in the final state are located at different atomic sites.Comment: 6 pages, 2 figures. arXiv admin note: text overlap with arXiv:1906.0812

Validation of the German version of the STarT-Back Tool (STarT-G): a cohort study with patients from primary care practices

Background: Current research emphasizes the high prevalence and costs of low back pain (LBP). The STarT Back Tool was designed to support primary care decision making for treatment by helping to determine the treatment prognosis of patients with non-specific low back pain. The German version is the STarT-G. The cross-cultural translation of the tool followed a structured and widely accepted process but to date it was only partially validated with a small sample. The aim of the study was to test the psychometric properties construct validity, discriminative ability, internal consistency and test-retest-reliability of the STarT-G and to compare them with values given for the original English version. Methods: A consecutive cohort study with a two-week retest was conducted among patients with non-specific LBP, aged 18 to 60 years, from primary care practices. Questionnaires were collected before the first consultation, and two weeks later by post, using the following reference standards: the Roland and Morris disability questionnaire, the Tampa Scale of Kinesiophobia, the Pain Catastrophizing Scale and the Hospital Anxiety and Depression Scale. Psychometric properties examined included the tool’s discriminative abilities, whether the psychosocial subscale was one factor, internal consistency, item redundancy, test-retest reliability and floor and ceiling effects. Results: There were 228 patients recruited with a mean age of 42.2 (SD 11.0) years, and 53 % were female. The areas under the curve (AUC) for discriminative ability ranged from 0.70 (STarT-G Subscale - Pain Catastrophizing Scale; CI95 0.63, 0.78) to 0.77 (STarT-G Total - Composite reference standard, CI95 0.60, 0.94). Factor loadings ranged from 0.49 to 0.74. Cronbach’s alpha testing the internal consistency and redundancy for the total/subscale scores were α = 0.52/0.55 respectively. The STarT-G test-retest reliability Kappa values for the total/subscale scores were 0.67/0.68 respectively. No floor or ceiling effects were present. Conclusions: The STarT-G shows acceptable psychometric properties although not in exact agreement with the original English version. The items previously regarded as a psychosocial subscale may be better seen as an index of different individual psychosocial constructs. The relevance of using the tool at the point of consultation should be further examined

AMPA receptors and seizures mediate hippocampal radial glia-like stem cell proliferation.

Neurogenesis is sustained throughout life in the mammalian brain, supporting hippocampus-dependent learning and memory. Its permanent alteration by status epilepticus (SE) is associated with learning and cognitive impairments. The mechanisms underlying the initiation of altered neurogenesis after SE are not understood. Glial fibrillary acidic protein-positive radial glia (RG)-like cells proliferate early after SE, but their proliferation dynamics and signaling are largely unclear. We have previously reported a polarized distribution of AMPA receptors (AMPARs) on RG-like cells in vivo and postulated that these may signal their proliferation. Here, we examined the acute effects of kainate on hippocampal precursor cells in vitro and in kainate-induced SE on proliferating and quiescent clones of 5-bromo-2-deoxyuridine prelabeled hippocampal precursors in vivo. In vitro, we found that 5 μM kainate shortened the cell cycle time of RG-like cells via AMPAR activation and accelerated cell cycle re-entry of their progeny. It also shifted their fate choice expanding the population of RG-like cells and reducing the population of downstream amplifying neural progenitors. Kainate enhanced the survival of all precursor cell subtypes. Pharmacologically, kainate's proliferative and survival effects were abolished by AMPAR blockade. Functional AMPAR expression was confirmed on RG-like cells in vitro. In agreement with these observations, kainate/seizures enhanced the proliferation and expansion predominantly of constitutively cycling RG-like cell clones in vivo. Our results identify AMPARs as key potential players in initiating the proliferation of dentate RG-like cells and unravel a possible receptor target for modifying the radial glia-like cell response to SE

Oligodendrocytes in the mouse corpus callosum maintain axonal function by delivery of glucose

In the optic nerve, oligodendrocytes maintain axonal function by supplying lactate as an energy substrate. Here, we report that, in acute brain slices of the mouse corpus callosum, exogenous glucose deprivation (EGD) abolished compound action potentials (CAPs), which neither lactate nor pyruvate could prevent. Loading an oligodendrocyte with 20 mM glucose using a patch pipette prevented EGD-mediated CAP reduction in about 70% of experiments. Loading oligodendrocytes with lactate rescued CAPs less efficiently than glucose. In mice lacking connexin 47, oligodendrocyte filling with glucose did not prevent CAP loss, emphasizing the importance of glial networks for axonal energy supply. Compared with the optic nerve, the astrocyte network in the corpus callosum was less dense, and loading astrocytes with glucose did not prevent CAP loss during EGD. We suggest that callosal oligodendrocyte networks provide energy to sustain axonal function predominantly by glucose delivery, and mechanisms of metabolic support vary across different white matter regions

Astrocytes and oligodendrocytes in the thalamus jointly maintain synaptic activity by supplying metabolites

Thalamic astrocytes and oligodendrocytes are coupled via gap junctions and form panglial networks. Here, we show that these networks have a key role in energy supply of neurons. Filling an astrocyte or an oligodendrocyte in acute slices with glucose or lactate is sufficient to rescue the decline of stimulation-induced field post-synaptic potential (fPSP) amplitudes during extracellular glucose deprivation (EGD). In mice lacking oligodendroglial coupling, loading an astrocyte with glucose does not rescue the EGD-mediated loss of fPSPs. Monocarboxylate and glucose transporters are required for rescuing synaptic activity during EGD. In mice deficient in astrocyte coupling, filling of an oligodendrocyte with glucose does not rescue fPSPs during EGD. Our results demonstrate that, in the thalamus, astrocytes and oligodendrocytes are jointly engaged in delivering energy substrates for sustaining neuronal activity and suggest that oligodendrocytes exert their effect mainly by assisting astrocytes in metabolite transfer to the postsynapse

Nuclear-fission studies with relativistic secondary beams: analysis of fission channels

Nuclear fission of several neutron-deficient actinides and pre-actinides from excitation energies around 11 MeV was studied at GSI Darmstadt by use of relativistic secondary beams. The characteristics of multimodal fission of nuclei around 226Th are systematically investigated and interpreted as the superposition of three fission channels. Properties of these fission channels have been determined for 15 systems. A global view on the properties of fission channels including previous results is presented. The positions of the asymmetric fission channels are found to be constant in element number over the whole range of systems investigated.Comment: 16 pages, 3 figures, background information on http://www.gsi.de/charm

Author's personal copy LAMINAR-SPECIFIC AND DEVELOPMENTAL EXPRESSION OF AQUAPORIN-4 IN THE MOUSE HIPPOCAMPUS

Abstract-Mice deficient in the water channel aquaporin-4 (AQP4) demonstrate increased seizure duration in response to hippocampal stimulation as well as impaired extracellular K ؉ clearance. However, the expression of AQP4 in the hippocampus is not well described. In this study, we investigated (i) the developmental, laminar and cell-type specificity of AQP4 expression in the hippocampus; (ii) the effect of Kir4.1 deletion on AQP4 expression; and (iii) performed Western blot and RT-PCR analyses. AQP4 immunohistochemistry on coronal sections from wild-type (WT) or Kir4.1 ؊/؊ mice revealed a developmentally-regulated and laminar-specific pattern, with highest expression in the CA1 stratum lacunosum-moleculare (SLM) and the molecular layer (ML) of the dentate gyrus (DG). AQP4 was colocalized with the glial markers glial fibrillary acidic protein (GFAP) and S100␤ in the hippocampus, and was also ubiquitously expressed on astrocytic endfeet around blood vessels. No difference in AQP4 immunoreactivity was observed in Kir4.1 ؊/؊ mice. Electrophysiological and postrecording RT-PCR analyses of individual cells revealed that AQP4 and Kir4.1 were co-expressed in nearly all CA1 astrocytes. In NG2 cells, AQP4 was also expressed at the transcript level. This study is the first to examine subregional AQP4 expression during development of the hippocampus. The strikingly high expression of AQP4 in the CA1 SLM and DG ML identifies these regions as potential sites of astrocytic K ؉ and H 2 O regulation. These results begin to delineate the functional capabilities of hippocampal subregions and cell types for K ؉ and H 2 O homeostasis, which is critical to excitability and serves as a potential target for modulation in diverse diseases

Electromagnetic-induced fission of 238U projectile fragments, a test case for the production of spherical super-heavy nuclei

Isotopic series of 58 neutron-deficient secondary projectiles (205,206At, 205-209Rn, 208-212,217,218Fr, 211-223Ra, 215-226Ac, 221-229Th, 226-231Pa, 231-234U) were produced by projectile fragmentation using a 1 A GeV 238U beam. Cross sections of fission induced by nuclear and electromagnetic interactions in a secondary lead target were measured. They were found to vary smoothly as a function of proton and neutron number of the fissioning system, also for nuclei with large ground-state shell effects near the 126-neutron shell. No stabilization against fission was observed for these nuclei at low excitation energies. Consequences for the expectations on the production cross sections of super-heavy nuclei are discussed.Comment: 20 pages, 13 figure

Limits on the production of direct photons in 200 A GeV32^{32}S + Au collisions

A search for the production of direct photons in S+Au collisions at 200\cdotA~GeV has been carried out in the CERN-WA80 experiment. For central collisions the measured photon excess at each p_T, averaged over the range 0.5~GeV/c~ \leq p_T \leq 2.5~GeV/c, corresponded to 5.0\% of the total inclusive photon yield with a statistical error of \sigma_{\rm stat}=0.8\% and a systematic error of \sigma_{\rm syst}=5.8\%. Upper limits on the invariant yield for direct photon production at the 90\%~C.L. are presented. Possible implications for the dynamics of high-energy heavy-ion collisions are discussed

Reactive astrocyte nomenclature, definitions, and future directions

Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters-preferably in vivo-plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions