Atomic and Electronic Structures of Unreconstructed Polar MgO(111) Thin Film on Ag(111)

Atomic and electronic structures of a polar surface of MgO formed on Ag(111) was investigated by using reflection high energy electron diffraction (RHEED), Auger electron spectroscopy, electron energy loss spectroscopy (EELS), and ultraviolet photoemission spectroscopy (UPS). A rather flat unreconstructed polar MgO(111) 1$\times$1 surface could be grown by alternate adsorption of Mg and O$_{2}$ on Ag(111). The stability of the MgO(111) surface was discussed in terms of interaction between Ag and Mg atoms at the interface, and charge state of the surface atoms. EELS of this surface did not show a band gap region, and finite density of states appeared at the Fermi level in UPS. These results suggest that a polar MgO(111) surface was not an insulating surface but a semiconducting or metallic surface.Comment: 6 figures, to be published in Phys. Rev.

The deleted in brachydactyly B domain of ROR2 is required for receptor activation by recruitment of Src

The transmembrane receptor 'ROR2' resembles members of the receptor tyrosine kinase family of signalling receptors in sequence but its' signal transduction mechanisms remain enigmatic. This problem has particular importance because mutations in ROR2 are associated with two human skeletal dysmorphology syndromes, recessive Robinow Syndrome (RS) and dominant acting Brachydactyly type B (BDB). Here we show, using a constitutive dimerisation approach, that ROR2 exhibits dimerisation-induced tyrosine kinase activity and the ROR2 C-terminal domain, which is deleted in BDB, is required for recruitment and activation of the non-receptor tyrosine kinase Src. Native ROR2 phosphorylation is induced by the ligand Wnt5a and is blocked by pharmacological inhibition of Src kinase activity. Eight sites of Src-mediated ROR2 phosphorylation have been identified by mass spectrometry. Activation via tyrosine phosphorylation of ROR2 receptor leads to its internalisation into Rab5 positive endosomes. These findings show that BDB mutant receptors are defective in kinase activation as a result of failure to recruit Src

Supersymmetry and Generic BSM Models in PYTHIA 8

We describe the implementation of supersymmetric models in PYTHIA 8, including production and decay of superparticles and allowing for violation of flavour, CP, and R-parity. We also present a framework for importing generic new-physics matrix elements into PYTHIA 8, in a way suitable for use with automated tools. We emphasize that this possibility should not be viewed as the only way to implement new-physics models in PYTHIA 8, but merely as an additional possibility on top of the already existing ones. Finally we address parton showers in exotic colour topologies, in particular ones involving colour epsilon tensors and colour sextets.Comment: 20 page

Kinesin light chain-1 serine-460 phosphorylation is altered in Alzheimer's disease and regulates axonal transport and processing of the amyloid precursor protein

Damage to axonal transport is an early pathogenic event in Alzheimer's disease. The amyloid precursor protein (APP) is a key axonal transport cargo since disruption to APP transport promotes amyloidogenic processing of APP. Moreover, altered APP processing itself disrupts axonal transport. The mechanisms that regulate axonal transport of APP are therefore directly relevant to Alzheimer's disease pathogenesis. APP is transported anterogradely through axons on kinesin-1 motors and one route for this transport involves calsyntenin-1, a type-1 membrane spanning protein that acts as a direct ligand for kinesin-1 light chains (KLCs). Thus, loss of calsyntenin-1 disrupts APP axonal transport and promotes amyloidogenic processing of APP. Phosphorylation of KLC1 on serine-460 has been shown to reduce anterograde axonal transport of calsyntenin-1 by inhibiting the KLC1-calsyntenin-1 interaction. Here we demonstrate that in Alzheimer's disease frontal cortex, KLC1 levels are reduced and the relative levels of KLC1 serine-460 phosphorylation are increased; these changes occur relatively early in the disease process. We also show that a KLC1 serine-460 phosphomimetic mutant inhibits axonal transport of APP in both mammalian neurons in culture and in Drosophila neurons in vivo. Finally, we demonstrate that expression of the KLC1 serine-460 phosphomimetic mutant promotes amyloidogenic processing of APP. Together, these results suggest that increased KLC1 serine-460 phosphorylation contributes to Alzheimer's disease

R-parity violating resonant stop production at the Large Hadron Collider

We have investigated the resonant production of a stop at the Large Hadron Collider, driven by baryon number violating interactions in supersymmetry. We work in the framework of minimal supergravity models with the lightest neutralino being the lightest supersymmetric particle which decays within the detector. We look at various dilepton and trilepton final states, with or without b-tags. A detailed background simulation is performed, and all possible decay modes of the lighter stop are taken into account. We find that higher stop masses are sometimes easier to probe, through the decay of the stop into the third or fourth neutralino and their subsequent cascades. We also comment on the detectability of such signals during the 7 TeV run, where, as expected, only relatively light stops can be probed. Our conclusion is that the resonant process may be probed, at both 10 and 14 TeV, with the R-parity violating coupling {\lambda}"_{312} as low as 0.05, for a stop mass of about 1 TeV. The possibility of distinguishing between resonant stop production and pair-production is also discussed.Comment: 20 pages, 4 figures, 6 tables; Version accepted by JHE

Revealing the molecular signatures of host-pathogen interactions.

Advances in sequencing technology and genome-wide association studies are now revealing the complex interactions between hosts and pathogen through genomic variation signatures, which arise from evolutionary co-existence

Constraints on supersymmetry with light third family from LHC data

We present a re-interpretation of the recent ATLAS limits on supersymmetry in channels with jets (with and without b-tags) and missing energy, in the context of light third family squarks, while the first two squark families are inaccessible at the 7 TeV run of the Large Hadron Collider (LHC). In contrast to interpretations in terms of the high-scale based constrained minimal supersymmetric standard model (CMSSM), we primarily use the low-scale parametrisation of the phenomenological MSSM (pMSSM), and translate the limits in terms of physical masses of the third family squarks. Side by side, we also investigate the limits in terms of high-scale scalar non-universality, both with and without low-mass sleptons. Our conclusion is that the limits based on 0-lepton channels are not altered by the mass-scale of sleptons, and can be considered more or less model-independent.Comment: 20 pages, 8 figures, 2 tables. Version published in JHE

Predicting outcome in acute stroke with large vessel occlusion:application and validation of MR PREDICTS in the ESCAPE-NA1 population

Background: Predicting outcome after endovascular treatment for acute ischemic stroke is challenging. We aim to investigate differences between predicted and observed outcomes in patients with acute ischemic stroke treated with endovascular treatment and to evaluate the performance of a validated outcome prediction score. Patients and methods: MR PREDICTS is an outcome prediction tool based on a logistic regression model designed to predict the treatment benefit of endovascular treatment based on the MR CLEAN and HERMES populations. ESCAPE-NA1 is a randomized trial of nerinetide vs. placebo in patients with acute stroke and large vessel occlusion. We applied MR PREDICTS to patients in the control arm of ESCAPE-NA1. Model performance was assessed by calculating its discriminative ability and calibration. Results: Overall, 556/1105 patients (50.3%) in the ESCAPE-NA1-trial were randomized to the control arm, 435/556 (78.2%) were treated within 6 h of symptom onset. Good outcome (modified Rankin scale 0–2) at 3 months was achieved in 275/435 patients (63.2%), the predicted probability of good outcome was 52.5%. Baseline characteristics were similar in the study and model derivation cohort except for age (ESCAPE-NA1: mean: 70 y vs. HERMES: 66 y), hypertension (72% vs. 57%), and collaterals (good collaterals, 15% vs. 44%). Compared to HERMES we observed higher rates of successful reperfusion (TICI 2b-3, ESCAPE-NA1: 87% vs. HERMES: 71%) and faster times from symptom onset to reperfusion (median: 201 min vs. 286 min). Model performance was good, indicated by a c-statistic of 0.76 (95%confidence interval: 0.71–0.81). Conclusion: Outcome-prediction using models created from HERMES data, based on information available in the emergency department underestimated the actual outcome in patients with acute ischemic stroke and large vessel occlusion receiving endovascular treatment despite overall good model performance, which might be explained by differences in quality of and time to reperfusion. These findings underline the importance of timely and successful reperfusion for functional outcomes in acute stroke patients.</p