Ice XII in its second regime of metastability

We present neutron powder diffraction results which give unambiguous evidence for the formation of the recently identified new crystalline ice phase[Lobban et al.,Nature, 391, 268, (1998)], labeled ice XII, at completely different conditions. Ice XII is produced here by compressing hexagonal ice I_h at T = 77, 100, 140 and 160 K up to 1.8 GPa. It can be maintained at ambient pressure in the temperature range 1.5 < T < 135 K. High resolution diffraction is carried out at T = 1.5 K and ambient pressure on ice XII and accurate structural properties are obtained from Rietveld refinement. At T = 140 and 160 K additionally ice III/IX is formed. The increasing amount of ice III/IX with increasing temperature gives an upper limit of T ~ 150 K for the successful formation of ice XII with the presented procedure.Comment: 3 Pages of RevTeX, 3 tables, 3 figures (submitted to Physical Review Letters

A topological insulator surface under strong Coulomb, magnetic and disorder perturbations

Three dimensional topological insulators embody a newly discovered state of matter characterized by conducting spin-momentum locked surface states that span the bulk band gap as demonstrated via spin-resolved ARPES measurements . This highly unusual surface environment provides a rich ground for the discovery of novel physical phenomena. Here we present the first controlled study of the topological insulator surfaces under strong Coulomb, magnetic and disorder perturbations. We have used interaction of iron, with a large Coulomb state and significant magnetic moment as a probe to \textit{systematically test the robustness} of the topological surface states of the model topological insulator Bi$_2$Se$_3$. We observe that strong perturbation leads to the creation of odd multiples of Dirac fermions and that magnetic interactions break time reversal symmetry in the presence of band hybridization. We also present a theoretical model to account for the altered surface of Bi$_2$Se$_3$. Taken collectively, these results are a critical guide in manipulating topological surfaces for probing fundamental physics or developing device applications.Comment: 14 pages, 4 Figures. arXiv admin note: substantial text overlap with arXiv:1009.621

The genome of Streptococcus pneumoniae is organized in topology-reacting gene clusters

The transcriptional response of Streptococcus pneumoniae was examined after exposure to the GyrB-inhibitor novobiocin. Topoisomer distributions of an internal plasmid confirmed DNA relaxation and recovery of the native level of supercoiling at low novobiocin concentrations. This was due to the up-regulation of DNA gyrase and the down-regulation of topoisomerases I and IV. In addition, >13% of the genome exhibited relaxation-dependent transcription. The majority of the responsive genes (>68%) fell into 15 physical clusters (14.6–85.6 kb) that underwent coordinated regulation, independently of operon organization. These genomic clusters correlated with AT content and codon composition, showing the chromosome to be organized into topology-reacting gene clusters that respond to DNA supercoiling. In particular, down-regulated clusters were flanked by 11–40 kb AT-rich zones that might have a putative structural function. This is the first case where genes responding to changes in the level of supercoiling in a coordinated manner were found organized as functional clusters. Such an organization revealed DNA supercoiling as a general feature that controls gene expression superimposed on other kinds of more specific regulatory mechanisms

Pre-implant right ventricular function might be an important predictor of the response to cardiac resynchronization therapy

<p>Abstract</p> <p>Objective</p> <p>Cardiac resynchronization therapy is proven efficacious in patients with heart failure (HF). Presence of biventricular HF is associated with a worse prognosis than having only left ventricular (LV) HF and pacing might deteriorate heart function. The aim of the study was to assess a possible significance of right ventricular (RV) pre-implant systolic function to predict response to CRT.</p> <p>Design</p> <p>We studied 22 HF-patients aged 72 ± 11 years, QRS-duration 155 ± 20 ms and with an LV ejection fraction (EF) of 26 ± 6% before and four weeks after receiving a CRT-device.</p> <p>Results</p> <p>There were no changes in LV diameters or end systolic volume (ESV) during the study. However, end diastolic volume (EDV) decreased from 226 ± 71 to 211 ± 64 ml (p = 0.02) and systolic maximal velocities (SMV) increased from 2.2 ± 0.4 to 2.6 ± 0.9 cm/s (p = 0.04). Pre-implant RV-SMV (6.2 ± 2.6 cm/s) predicted postoperative increase in LV contractility, p = 0.032.</p> <p>Conclusions</p> <p>Pre-implant decreased RV systolic function might be an important way to predict a poor response to CRT implicating that other treatments should be considered. Furthermore we found that 3D- echocardiography and Tissue Doppler Imaging were feasible to detect short-term changes in LV function.</p

Resolving the ancestry of Austronesian-speaking populations

There are two very different interpretations of the prehistory of Island Southeast Asia (ISEA), with genetic evidence invoked in support of both. The “out-of-Taiwan” model proposes a major Late Holocene expansion of Neolithic Austronesian speakers from Taiwan. An alternative, proposing that Late Glacial/postglacial sea-level rises triggered largely autochthonous dispersals, accounts for some otherwise enigmatic genetic patterns, but fails to explain the Austronesian language dispersal. Combining mitochondrial DNA (mtDNA), Y-chromosome and genome-wide data, we performed the most comprehensive analysis of the region to date, obtaining highly consistent results across all three systems and allowing us to reconcile the models. We infer a primarily common ancestry for Taiwan/ISEA populations established before the Neolithic, but also detected clear signals of two minor Late Holocene migrations, probably representing Neolithic input from both Mainland Southeast Asia and South China, via Taiwan. This latter may therefore have mediated the Austronesian language dispersal, implying small-scale migration and language shift rather than large-scale expansion

Bonding and the agency risk premium: An analysis of migrations between the AIM and the Official List of the London Stock Exchange

Firms that change their listing from the less regulated AIM to the more regulated main section of the London Stock Exchange exhibit positive abnormal returns on the announcement day. For firms moving in the opposite direction, both announcement and implementation day abnormal returns are negative. Following implementation, the pattern is reversed for both categories of firm. We show that differences in liquidity, conventional risk factors and in medium to long term firm survival rates between the two listing regimes do not explain the observed patterns of returns, suggesting that the answer lies in the different bonding requirements of the two market segments and an agency risk premium.JEL Codes: G12, G14, G15, G30, G32, G3

Prolonged mitotic arrest induces a caspase-dependent DNA damage response at telomeres that determines cell survival

A delay in the completion of metaphase induces a stress response that inhibits further cell proliferation or induces apoptosis. This response is thought to protect against genomic instability and is important for the effects of anti-mitotic cancer drugs. Here, we show that mitotic arrest induces a caspase-dependent DNA damage response (DDR) at telomeres in non-apoptotic cells. This pathway is under the control of Mcl-1 and other Bcl-2 family proteins and requires caspase-9, caspase-3/7 and the endonuclease CAD/DFF40. The gradual caspase-dependent loss of the shelterin complex protein TRF2 from telomeres promotes a DDR that involves DNA-dependent protein kinase (DNA-PK). Suppression of mitotic telomere damage by enhanced expression of TRF2, or the inhibition of either caspase-3/7 or DNA-PK during mitotic arrest, promotes subsequent cell survival. Thus, we demonstrate that mitotic stress is characterised by the sub-apoptotic activation of a classical caspase pathway, which promotes telomere deprotection, activates DNA damage signalling, and determines cell fate in response to a prolonged delay in mitosis