International money supply and real estate risk premium: The case of the London office market

The main purpose of this study is to deeply investigate the determinants of the risk premium for the Central London market between Q2-2002 and Q3-2015 using a vector autoregression (VAR) model. We shed new light on the role of central banks in the historical level of the commercial real estate risk premium. Indeed, since the global financial crisis (GFC), central banks have used unconventional monetary policies, increasing the quantity of money available in the economy and creating structural changes. Therefore, we have described the link between monetary policies and real estate using a theoretical IS/LM Mundell-Fleming framework for a small open economy with a flexible exchange rate. To empirically explore this phenomenon, we have constructed a monetary index adapted to the office market. We find that throughout the whole period (2002–2015), the vacancy rate, the employment in services, the FTSE 100, the new monetary index and the autoregressive parameter are the main determinants of the historical risk premium. However, this result hides the complex realities of different sub-periods. Finally, we study the structural changes introduced by the monetary policy using a structural VAR model and impulse-response function

A role for protein phosphatase PP1γ in SMN complex formation and subnuclear localization to Cajal bodies

The spinal muscular atrophy (SMA) gene product SMN forms with gem-associated protein 2-8 (Gemin2-8) and unrip (also known as STRAP) the ubiquitous survival motor neuron (SMN) complex, which is required for the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs), their nuclear import and their localization to subnuclear domain Cajal bodies (CBs). The concentration of the SMN complex and snRNPs in CBs is reduced upon SMN deficiency in SMA cells. Subcellular localization of the SMN complex is regulated in a phosphorylation-dependent manner and the precise mechanisms remain poorly understood. Using co-immunoprecipitation in HeLa cell extracts and in vitro protein binding assays, we show here that the SMN complex and its component Gemin8 interact directly with protein phosphatase PP1γ. Overexpression of Gemin8 in cells increases the number of CBs and results in targeting of PP1γ to CBs. Moreover, depletion of PP1γ by RNA interference enhances the localization of the SMN complex and snRNPs to CBs. Consequently, the interaction between SMN and Gemin8 increases in cytoplasmic and nuclear extracts of PP1γ-depleted cells. Two-dimensional protein gel electrophoresis revealed that SMN is hyperphosphorylated in nuclear extracts of PP1γ-depleted cells and expression of PP1γ restores these isoforms. Notably, SMN deficiency in SMA leads to the aberrant subcellular localization of Gemin8 and PP1γ in the atrophic skeletal muscles, suggesting that the function of PP1γ is likely to be affected in disease. Our findings reveal a role of PP1γ in the formation of the SMN complex and the maintenance of CB integrity. Finally, we propose Gemin8 interaction with PP1γ as a target for therapeutic intervention in SMA

Distinct domains of the spinal muscular atrophy protein SMN are required for targeting to Cajal bodies in mammalian cells.

Mutations of the survival motor neuron gene SMN1 cause the inherited disease spinal muscular atrophy (SMA). The ubiquitous SMN protein facilitates the biogenesis of spliceosomal small nuclear ribonucleoproteins (snRNPs). The protein is detected in the cytoplasm, nucleoplasm and enriched with snRNPs in nuclear Cajal bodies. It is structurally divided into at least an amino-terminal region rich in basic amino acid residues, a central Tudor domain, a self-association tyrosine-glycine-box and an exon7-encoded C-terminus. To examine the domains required for the intranuclear localization of SMN, we have used fluorescently tagged protein mutants transiently overexpressed in mammalian cells. The basic amino acid residues direct nucleolar localization of SMN mutants. The Tudor domain promotes localization of proteins in the nucleus and it cooperates with the basic amino acid residues and the tyrosine-glycine-box for protein localization in Cajal bodies. Moreover, the most frequent disease-linked mutant SMN{Delta}ex7 reduces accumulation of snRNPs in Cajal bodies, suggesting that the C-terminus of SMN participates in targeting to Cajal bodies. A reduced number of Cajal bodies in patient fibroblasts associates with the absence of snRNPs in Cajal bodies, revealing that intranuclear snRNA organization is modified in disease. These results indicate that direct and indirect mechanisms regulate localization of SMN in Cajal bodies

Electron localization by a donor in the vicinity of a basal stacking fault in GaN

We study the effects of the vicinity between a shallow donor nucleus and an I1-type basal stacking fault (BSF) in GaN. We propose a numerical calculation, in the “effective potential” formalism, of energies and envelope functions of electrons submitted to the conjunction of attractive potentials caused by the BSF and the donor. We show that the donor localizes the electron along the plane of the BSF, even when the donor lies as far as 10 nm from the BSF. Conversely, the presence of the BSF enhances the donor binding energy by up to a factor of 1.8, when the donor is placed exactly on the BSF. We briefly discuss the probability of occurrence of such a situation in, e.g., a-plane GaN, as well as its consequences on transport and optical properties of this material

Impact of biexcitons on the relaxation mechanisms of polaritons in III-nitride based multiple quantum well microcavities

We report on the direct observation of biexcitons in a III nitride based multiple quantum well microcavity operating in the strong light-matter coupling regime by means of nonresonant continuous wave and time-resolved photoluminescence at low temperature. First, the biexciton dynamics is investigated for the bare active medium (multiple quantum wells alone) evidencing localization on potential fluctuations due to alloy disorder and thermalization between both localized and free excitonic and biexcitonic populations. Then, the role of biexcitons is considered for the full microcavity: in particular, we observe that for specific detunings the bottom of the lower polariton branch is directly fed by the radiative dissociation of either cavity biexcitons or excitons mediated by one LO-phonon. Accordingly, minimum polariton lasing thresholds are observed, when the bottom of the lower polariton branch corresponds in energy to the exciton or cavity biexciton first LO-phonon replica. This singular observation highlights the role of excitonic molecules in the polariton condensate formation process as being a more efficient relaxation channel when compared to the usually assumed acoustical phonon emission one.This work was supported by the NCCR Quantum Photonics, research instrument of the Swiss National Science Foundation, through Grant No. 129715 and Grant No. 200020-113542, and by the EU-project Clermont4 (Grant No. FP7-235114)

Time-resolved spectroscopy on GaN nanocolumns grown by plasma assisted molecular beam epitaxy on Si substrates

A detailed study of excitons in unstrained GaN nanocolumns grown by plasma assisted molecular beam epitaxy on silicon substrates is presented. The time-integrated and time-resolved photoluminescence spectra do not depend significantly on the (111) or (001) Si surface used. However, an unusually high relative intensity of the two-electron satellite peak of the dominant donor-bound exciton line is systematically observed. We correlate this observation with the nanocolumn morphology determined by scanning electron microscopy, and therefore propose an interpretation based on the alteration of wave functions of excitonic complexes and of donor states by the proximity of the semiconductor surface. This explanation is supported by a model that qualitatively accounts for both relative intensities and time decays of the photoluminescence lines. ©2009 American Institute of Physic

Low-temperature time-resolved cathodoluminescence study of exciton dynamics involving basal stacking faults in a-plane GaN

Time-resolved cathodoluminescence at 27 K has been performed on a-plane GaN grown by epitaxial lateral overgrowth. We detail the relaxation and recombination mechanisms of excitons [free or bound to neutral donors, or bound to I1-type basal stacking faults (BSFs)] in relation to the local density in BSFs. We describe the slow exciton capture rate on isolated BSFs by a diffusion model involving donors via a hopping process. Where BSFs are organized into bundles, we relate the shorter rise time to intra-BSF localization processes and the multiexponential decay to the type-II band alignment of BSFs in wurtzite GaN

Exciton localization on basal stacking faults in a-plane epitaxial lateral overgrown GaN grown by hydride vapor phase epitaxy

We present a detailed study of the luminescence at 3.42 eV usually observed in a-plane epitaxial lateral overgrowth (ELO) GaN grown by hydride vapor phase epitaxy on r-plane sapphire. This band is related to radiative recombination of excitons in a commonly encountered extended defect of a-plane GaN: I-1 basal stacking fault. Cathodoluminescence measurements show that these stacking faults are essentially located in the windows and the N-face wings of the ELO-GaN and that they can appear isolated as well as organized into bundles. Time-integrated and time-resolved photoluminescence, supported by a qualitative model, evidence not only the efficient trapping of free excitons (FXs) by basal plane stacking faults but also some localization inside I-1 stacking faults themselves. Measurements at room temperature show that FXs recombine efficiently with rather long luminescence decay times (360 ps), comparable to those encountered in high-quality GaN epilayers. We discuss the possible role of I-1 stacking faults in the overall recombination mechanism of excitons

Intrinsic dynamics of weakly and strongly confined excitons in nonpolar nitride-based heterostructures

Both weakly and strongly confined excitons are studied by time-resolved photoluminescence in a nonpolar nitride-based heterostructure grown by molecular beam epitaxy on the a-facet of a bulk GaN crystal, with an ultralow dislocation density of 2 × 105 cm-2. Strong confinement is obtained in a 4 nm thick Al0.06Ga0.94N/GaN quantum well (QW), whereas weakly confined exciton-polaritons are observed in a 200 nm thick GaN epilayer. Thanks to the low dislocation density, the effective lifetime of strongly confined excitons increases between 10 and 150 K, proving the domination of radiative recombination processes. Above 150 K the QW emission lifetime diminishes, whereas the decay time of excitons in the barriers increases, until both barrier and QW exciton populations become fully thermalized at 300 K. We conclude that the radiative efficiency of our GaN QW at 300 K is limited by nonradiative recombinations in the barriers. The increase of exciton-polariton coherence lengths caused by low dislocation densities allows us to observe and model the quantized emission modes in the 200 nm nonpolar GaN layer. Finally, the low-temperature phonon-assisted relaxation mechanisms of such center-of-mass quantized exciton-polaritons are described

Patent Foramen Ovale Closure or Anticoagulation vs. Antiplatelets after Stroke

BACKGROUND Trials of patent foramen ovale (PFO) closure to prevent recurrent stroke have been inconclusive. We investigated whether patients with cryptogenic stroke and echocardiographic features representing risk of stroke would benefit from PFO closure or anticoagulation, as compared with antiplatelet therapy. METHODS In a multicenter, randomized, open-label trial, we assigned, in a 1:1:1 ratio, patients 16 to 60 years of age who had had a recent stroke attributed to PFO, with an associated atrial septal aneurysm or large interatrial shunt, to transcatheter PFO closure plus long-term antiplatelet therapy (PFO closure group), antiplatelet therapy alone (antiplatelet-only group), or oral anticoagulation (anticoagulation group) (randomization group 1). Patients with contraindications to anticoagulants or to PFO closure were randomly assigned to the alternative noncontraindicated treatment or to antiplatelet therapy (randomization groups 2 and 3). The primary outcome was occurrence of stroke. The comparison of PFO closure plus antiplatelet therapy with antiplatelet therapy alone was performed with combined data from randomization groups 1 and 2, and the comparison of oral anticoagulation with antiplatelet therapy alone was performed with combined data from randomization groups 1 and 3. RESULTS A total of 663 patients underwent randomization and were followed for a mean (+/- SD) of 5.3 +/- 2.0 years. In the analysis of randomization groups 1 and 2, no stroke occurred among the 238 patients in the PFO closure group, whereas stroke occurred in 14 of the 235 patients in the antiplatelet-only group (hazard ratio, 0.03; 95% confidence interval, 0 to 0.26; P<0.001). Procedural complications from PFO closure occurred in 14 patients (5.9%). The rate of atrial fibrillation was higher in the PFO closure group than in the antiplatelet-only group (4.6% vs. 0.9%, P = 0.02). The number of serious adverse events did not differ significantly between the treatment groups (P = 0.56). In the analysis of randomization groups 1 and 3, stroke occurred in 3 of 187 patients assigned to oral anticoagulants and in 7 of 174 patients assigned to antiplatelet therapy alone. CONCLUSIONS Among patients who had had a recent cryptogenic stroke attributed to PFO with an associated atrial septal aneurysm or large interatrial shunt, the rate of stroke recurrence was lower among those assigned to PFO closure combined with antiplatelet therapy than among those assigned to antiplatelet therapy alone. PFO closure was associated with an increased risk of atrial fibrillation