Multistage Zeeman deceleration of atomic and molecular oxygen

Multistage Zeeman deceleration is a technique used to reduce the velocity of neutral molecules with a magnetic dipole moment. Here we present a Zeeman decelerator that consists of 100 solenoids and 100 magnetic hexapoles, that is based on a short prototype design presented recently [Phys. Rev. A 95, 043415 (2017)]. The decelerator features a modular design with excellent thermal and vacuum properties, and is robustly operated at a 10 Hz repetition rate. This multistage Zeeman decelerator is particularly optimized to produce molecular beams for applications in crossed beam molecular scattering experiments. We characterize the decelerator using beams of atomic and molecular oxygen. For atomic oxygen, the magnetic fields produced by the solenoids are used to tune the final longitudinal velocity in the 500 - 125 m/s range, while for molecular oxygen the velocity is tunable in the 350 - 150 m/s range. This corresponds to a maximum kinetic energy reduction of 95% and 80% for atomic and molecular oxygen, respectively.Comment: Latest version as accepted by Physical Review

Design and construction of a multistage Zeeman decelerator for crossed molecular beams scattering experiments

Zeeman deceleration is a relatively new technique used to obtain full control over the velocity of paramagnetic atoms or molecules in a molecular beam. We present a detailed description of a multistage Zeeman decelerator that has recently become operational in our laboratory [Cremers \emph{et al.}, Phys. Rev. A 98, 033406 (2018)], and that is specifically optimized for crossed molecular beams scattering experiments. The decelerator consists of an alternating array of 100 solenoids and 100 permanent hexapoles to guide or decelerate beams of paramagnetic atoms or molecules. The Zeeman decelerator features a modular design that is mechanically easy to extend to arbitrary length, and allows for solenoid and hexapole elements that are convenient to replace. The solenoids and associated electronics are efficiently water cooled and allow the Zeeman decelerator to operate at repetition rates exceeding 10 Hz. We characterize the performance of the decelerator using various beams of metastable rare gas atoms. Imaging of the atoms that exit the Zeeman decelerator reveals the transverse focusing properties of the hexapole array in the Zeeman decelerator

Disruption of the basal body protein POC1B results in autosomal-recessive cone-rod dystrophy

Exome sequencing revealed a homozygous missense mutation (c.317C>G [p.Arg106Pro]) in POC1B, encoding POC1 centriolar protein B, in three siblings with autosomal-recessive cone dystrophy or cone-rod dystrophy and compound-heterozygous POC1B mutations (c.199_201del [p.G1n67del] and c.810+1G>T) in an unrelated person with cone-rod dystrophy. Upon overexpression of POC1B in human TERT-immortalized retinal pigment epithelium 1 cells, the encoded wild-type protein localized to the basal body of the primary cilium, whereas this localization was lost for p.Arg106Pro and p.G1n67del variant forms of POC1B. Morpholino-oligonucleotide-induced knockdown of poc1b translation in zebrafish resulted in a dose-dependent small-eye phenotype, impaired optokinetic responses, and decreased length of photoreceptor outer segments. These ocular phenotypes could partially be rescued by wild-type human POC1B mRNA, but not by c.199_201del and c.317C>G mutant human POC1B mRNAs. Yeast two-hybrid screening of a human retinal cDNA library revealed FAM161A as a binary interaction partner of POC1B. This was confirmed in coimmunoprecipitation and colocalization assays, which both showed loss of FAM161A interaction with p.Arg106Pro and p.G1n67del variant forms of POC1B. FAM161A was previously implicated in autosomal-recessive retinitis pigmentosa and shown to be located at the base of the photoreceptor connecting cilium, where it interacts with several other ciliopathy-associated proteins. Altogether, this study demonstrates that POC1B mutations result in a defect of the photoreceptor sensory cilium and thus affect cone and rod photoreceptors

The [FeFe] hydrogenase of Nyctotherus ovalis has a chimeric origin

BACKGROUND: The hydrogenosomes of the anaerobic ciliate Nyctotherus ovalis show how mitochondria can evolve into hydrogenosomes because they possess a mitochondrial genome and parts of an electron-transport chain on the one hand, and a hydrogenase on the other hand. The hydrogenase permits direct reoxidation of NADH because it consists of a [FeFe] hydrogenase module that is fused to two modules, which are homologous to the 24 kDa and the 51 kDa subunits of a mitochondrial complex I. RESULTS: The [FeFe] hydrogenase belongs to a clade of hydrogenases that are different from well-known eukaryotic hydrogenases. The 24 kDa and the 51 kDa modules are most closely related to homologous modules that function in bacterial [NiFe] hydrogenases. Paralogous, mitochondrial 24 kDa and 51 kDa modules function in the mitochondrial complex I in N. ovalis. The different hydrogenase modules have been fused to form a polyprotein that is targeted into the hydrogenosome. CONCLUSION: The hydrogenase and their associated modules have most likely been acquired by independent lateral gene transfer from different sources. This scenario for a concerted lateral gene transfer is in agreement with the evolution of the hydrogenosome from a genuine ciliate mitochondrion by evolutionary tinkering

Cytomorphology review of 100 newly diagnosed lower-risk MDS patients in the European LeukemiaNet MDS (EUMDS) registry reveals a high inter-observer concordance

Objectives To examine contemporary survival patterns in the general population of patients diagnosed with chronic myeloid leukaemia (CML), and to identify patient groups with less than optimal outcomes. Design Prospective population-based cohort. Setting The UK's Haematological Malignancy Research Network (catchment population 3.6 million, with >2000 new haematological malignancies diagnosed annually). Participants All patients newly diagnosed with CML, from September 2004 to August 2011 and followed up to 31 March 2013. Main outcome measure Incidence and survival. Results With a median diagnostic age of 59 years, the CML age standardised (European) incidence was 0.9/100 000 (95% CIs 0.8 to 0.9), 5-year overall survival was 78.9% (72.3 to 84.0) and 5-year relative survival 88.6% (81.0 to 93.3). The efficacy of treatment across all ages was clearly demonstrated; the relative survival curves for those under 60 and over 60 years being closely aligned. Survival findings were similar for men and women, but varied with deprivation; the age and sex adjusted HR being 3.43 (1.89 to 6.22) for deprivation categories 4–5 (less affluent) versus 1–3 (more affluent). None of these differences were attributable to the biological features of the disease. Conclusions When therapy is freely provided, population-based survival for CML is similar to that reported in clinical trials, and age loses its prognostic significance. However, although most of the patients with CML now experience close to normal lifespans, those living in more deprived areas tend to have poorer outcomes, despite receiving the same clinical care. A significant improvement in overall population outcomes could be achieved if these socioeconomic differences, which may reflect the treatment compliance, could be eliminated

Disruption of the Basal Body Protein POC1B Results in Autosomal-Recessive Cone-Rod Dystrophy

Exome sequencing revealed a homozygous missense mutation (c.317C>G [p.Arg106Pro]) in POC1B, encoding POC1 centriolar protein B, in three siblings with autosomal-recessive cone dystrophy or cone-rod dystrophy and compound-heterozygous POC1B mutations (c.199_201del [p.Gln67del] and c.810+1G>T) in an unrelated person with cone-rod dystrophy. Upon overexpression of POC1B in human TERT-immortalized retinal pigment epithelium 1 cells, the encoded wild-type protein localized to the basal body of the primary cilium, whereas this localization was lost for p.Arg106Pro and p.Gln67del variant forms of POC1B. Morpholino-oligonucleotide-induced knockdown of poc1b translation in zebrafish resulted in a dose-dependent small-eye phenotype, impaired optokinetic responses, and decreased length of photoreceptor outer segments. These ocular phenotypes could partially be rescued by wild-type human POC1B mRNA, but not by c.199_201del and c.317C>G mutant human POC1B mRNAs. Yeast two-hybrid screening of a human retinal cDNA library revealed FAM161A as a binary interaction partner of POC1B. This was confirmed in coimmunoprecipitation and colocalization assays, which both showed loss of FAM161A interaction with p.Arg106Pro and p.Gln67del variant forms of POC1B. FAM161A was previously implicated in autosomal-recessive retinitis pigmentosa and shown to be located at the base of the photoreceptor connecting cilium, where it interacts with several other ciliopathy-associated proteins. Altogether, this study demonstrates that POC1B mutations result in a defect of the photoreceptor sensory cilium and thus affect cone and rod photoreceptors

Numerical assessment of the impact of vehicle body stiffness on handling performance

This paper investigates the problem of how to use Computer-Aided Engineering (CAE) tools to properly assess the influence of vehicle body stiffness on handling performance. One of the challenges in this context is related to the accuracy of the Body-In-White (BIW) model. The amount of degrees of freedom should be minimal without losing the necessary accuracy, especially for local stiffness modifications. A technique for this is proposed that uses Component Mode Synthesis (CMS) methods to reduce a Finite Element (FE) model of a BIW. The resulting reduced model of the BIW is then used in flexible Multibody (MB) simulations of handling manoeuvres in order to investigate the influence of a changing body stiffness. For the objective handling evaluation, conventional metrics are assessed. However, because these metrics only show small differences for various body stiffnesses, also other quantities, such as body deformation, are proposed as a clearer indicator of the influence of vehicle body stiffness on handling performance.status: publishe

Complete Genome Sequence of Nitrospina watsonii 347, Isolated from the Black Sea

Project: PRJEB56043 Complete genome of Nitrospina watsonii Nb-347, a nitrite-oxidizing bacterium originally isolated from the Black Sea at 100 m dept