4,763 research outputs found

    Controlling fast transport of cold trapped ions

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    We realize fast transport of ions in a segmented micro-structured Paul trap. The ion is shuttled over a distance of more than 10^4 times its groundstate wavefunction size during only 5 motional cycles of the trap (280 micro meter in 3.6 micro seconds). Starting from a ground-state-cooled ion, we find an optimized transport such that the energy increase is as low as 0.10 ±\pm 0.01 motional quanta. In addition, we demonstrate that quantum information stored in a spin-motion entangled state is preserved throughout the transport. Shuttling operations are concatenated, as a proof-of-principle for the shuttling-based architecture to scalable ion trap quantum computing.Comment: 5 pages, 4 figure

    Aerosol Route to Antibacterial Nanosilver Coating of Cotton Fabrics

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    The paper describes a gas phase process for the preparation of cotton fabrics coated with silver nanoparticles as antimicrobial agents. Silver nanoparticles are synthesized by means of atmospheric pressure electrical discharges (spark discharge and glow discharge) in pure inert gases, and the aerosols are passed through cotton fabric samples, where nanoparticles deposit. The particle size distribution of the aerosols is measured online during synthesis. Also, the cristallinity, size and morphology of the silver particles are analyzed. The mean size of the primary particles of silver varies from 4 nm to 18 nm, depending upon the type of discharge, the nature and flow rate of the gas. The bactericidal activity of the cotton samples doped with silver nanoparticles is assessed following the ISO 20743 method. All cotton samples show significant bactericidal property, although it degrades with increasing primary particle size and particle agglomeration. This purely physical aerosol route is a promising sustainable method for nanocoating of textiles

    Improved bone defect healing by a superagonistic GDF5 variant derived from a patient with multiple synostoses syndrome

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    Multiple synostoses syndrome 2 (SYNS2) is a rare genetic disease characterized by multiple fusions of the joints of the extremities, like phalangeal joints, carpal and tarsal joints or the knee and elbows. SYNS2 is caused by point mutations in the Growth and Differentiation Factor 5 (GDF5), which plays an essential role during skeletal development and regeneration. We selected one of the SYNS2-causing GDF5 mutations, p.N445T, which is known to destabilize the interaction with the Bone Morphogenetic Protein (BMP) antagonist NOGGIN (NOG), in order to generate the superagonistic GDF5 variant GDF5(N445T). In this study, we tested its capacity to support regeneration in a rat critical-sized defect model in vivo. MicroCT and histological analyses indicate that GDF5(N445T)-treated defects show faster and more efficient healing compared to GDF5 wild type (GDF5(wt))-treated defects. Microarray-based gene expression and quantitative PCR analyses from callus tissue point to a specific acceleration of the early phases of bone healing, comprising the inflammation and chondrogenesis phase. These results support the concept that disease-deduced growth factor variants are promising lead structures for novel therapeutics with improved clinical activities

    The role of centrosome distal appendage proteins (DAPs) in nephronophthisis and ciliogenesis

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    The primary cilium is found in most mammalian cells and plays a functional role in tissue homeostasis and organ development by modulating key signaling pathways. Ciliopathies are a group of genetically heterogeneous disorders resulting from defects in cilia development and function. Patients with ciliopathic disorders exhibit a range of phenotypes that include nephronophthisis (NPHP), a progressive tubulointerstitial kidney disease that commonly results in end-stage renal disease (ESRD). In recent years, distal appendages (DAPs), which radially project from the distal end of the mother centriole, have been shown to play a vital role in primary ciliary vesicle docking and the initiation of ciliogenesis. Mutations in the genes encoding these proteins can result in either a complete loss of the primary cilium, abnormal ciliary formation, or defective ciliary signaling. DAPs deficiency in humans or mice commonly results in NPHP. In this review, we outline recent advances in our understanding of the molecular functions of DAPs and how they participate in nephronophthisis development

    Target structure independent 7Li^7\vec{Li} elastic scattering at low momentum transfers

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    Analyzing powers and cross sections for the elastic scattering of polarized 7Li by targets of 6Li, 7Li and 12C are shown to depend only on the properties of the projectile for momentum transfers of less than 1.0 fm-1. The result of a detailed analysis of the experimental data within the framework of the coupled channels model with ground state reorientation and transitions to the excited states of the projectile and targets included in the coupling schemes are presented. This work suggests that nuclear properties of weakly-bound nuclei can be tested by elastic scattering experiments, independent of the target used, if data are acquired for momentum transfers less than ~1.0 fm-1.Comment: 9 pages, 4 figures, 1 table, accepted in Phys. Lett.

    Entanglement, elasticity and viscous relaxation of actin solutions

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    We have investigated the viscosity and the plateau modulus of actin solutions with a magnetically driven rotating disc rheometer. For entangled solutions we observed a scaling of the plateau modulus versus concentration with a power of 7/5. The measured terminal relaxation time increases with a power 3/2 as a function of polymer length. We interpret the entanglement transition and the scaling of the plateau modulus in terms of the tube model for semiflexible polymers.Comment: 5 pages, 4 figures, published versio

    The centrosomal protein 83 (CEP83) regulates human pluripotent stem cell differentiation towards the kidney lineage

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    During embryonic development, the mesoderm undergoes patterning into diverse lineages including axial, paraxial, and lateral plate mesoderm (LPM). Within the LPM, the so-called intermediate mesoderm (IM) forms kidney and urogenital tract progenitor cells, while the remaining LPM forms cardiovascular, hematopoietic, mesothelial, and additional progenitor cells. The signals that regulate these early lineage decisions are incompletely understood. Here, we found that the centrosomal protein 83 (CEP83), a centriolar component necessary for primary cilia formation and mutated in pediatric kidney disease, influences the differentiation of human induced pluripotent stem cells (hiPSCs) towards intermediate mesoderm. We induced inactivating deletions of (CEP83) in hiPSCs and applied a 7 day in vitro protocol of intermediate mesoderm kidney progenitor differentiation, based on timed application of WNT and FGF agonists. We characterized induced mesodermal cell populations using single cell and bulk transcriptomics and tested their ability to form kidney structures in subsequent organoid culture. While hiPSCs with homozygous (CEP83) inactivation were normal regarding morphology and transcriptome, their induced differentiation into IM progenitor cells was perturbed. Mesodermal cells induced after 7 days of monolayer culture of (CEP83)-deficient hiPCS exhibited absent or elongated primary cilia, displayed decreased expression of critical IM genes ((PAX8), (EYA1), (HOXB7)), and an aberrant induction of LPM markers (e. g. (FOXF1), (FOXF2), (FENDRR), (HAND1) ,(HAND2)). Upon subsequent organoid culture, wildtype cells differentiated to form kidney tubules and glomerular-like structures, whereas (CEP83)-deficient cells failed to generate kidney cell types, instead upregulating cardiomyocyte, vascular, and more general LPM progenitor markers. Our data suggest that (CEP83) regulates the balance of intermediate mesoderm and lateral plate mesoderm formation from human pluripotent stem cells, identifying a potential link between centriolar or ciliary function and mesodermal lineage induction

    Disease overarching mechanisms that explain and predict outcome of patients with high cardiovascular risk: rationale and design of the Berlin Long-term Observation of vascular events (BeLOVE) study

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    BACKGROUND: Cardiovascular disease (CVD) is the leading cause of premature death worldwide. Effective and individualized treatment requires exact knowledge about both risk factors and risk estimation. Most evidence for risk prediction currently comes from population-based studies on first incident cardiovascular events. In contrast, little is known about the relevance of risk factors for the outcome of patients with established CVD or those who are at high risk of CVD, including patients with type 2 diabetes. In addition, most studies focus on individual diseases, whereas less is known about disease overarching risk factors and cross-over risk. AIM: The aim of BeLOVE is to improve short- and long-term prediction and mechanistic understanding of cardiovascular disease progression and outcomes in very high-risk patients, both in the acute as well as in the chronic phase, in order to provide the basis for improved, individualized management. STUDY DESIGN: BeLOVE is an observational prospective cohort study of patients of both sexes aged >18 in selected Berlin hospitals, who have a high risk of future cardiovascular events, including patients with a history of acute coronary syndrome (ACS), acute stroke (AS), acute heart failure (AHF), acute kidney injury (AKI) or type 2 diabetes with manifest target-organ damage. BeLOVE includes 2 subcohorts: The acute subcohort includes 6500 patients with ACS, AS, AHF, or AKI within 2-8 days after their qualifying event, who undergo a structured interview about medical history as well as blood sample collection. The chronic subcohort includes 6000 patients with ACS, AS, AHF, or AKI 90 days after event, and patients with type 2 diabetes (T2DM) and target-organ damage. These patients undergo a 6-8 hour deep phenotyping program, including detailed clinical phenotyping from a cardiological, neurological and metabolic perspective, questionnaires including patient-reported outcome measures (PROMs)as well as magnetic resonance imaging. Several biological samples are collected (i.e. blood, urine, saliva, stool) with blood samples collected in a fasting state, as well as after a metabolic challenge (either nutritional or cardiopulmonary exercise stress test). Ascertainment of major adverse cardiovascular events (MACE) will be performed in all patients using a combination of active and passive follow up procedures, such as on-site visits (if applicable), telephone interviews, review of medical charts, and links to local health authorities. Additional phenotyping visits are planned at 2, 5 and 10 years after inclusion into the chronic subcohort. FUTURE PERSPECTIVE: BeLOVE provides a unique opportunity to study both the short- and long-term disease course of patients at high cardiovascular risk through innovative and extensive deep phenotyping. Moreover, the unique study design provides opportunities for acute and post-acute inclusion and allows us to derive two non-nested yet overlapping sub-cohorts, tailored for upcoming research questions. Thereby, we aim to study disease overarching research questions, to understand crossover risk, and to find similarities and differences between clinical phenotypes of patients at high cardiovascular risk

    CaB_6: a new semiconducting material for spin electronics

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    Ferromagnetism was recently observed at unexpectedly high temperatures in La-doped CaB_6. The starting point of all theoretical proposals to explain this observation is a semimetallic electronic structure calculated for CaB_6 within the local density approximation. Here we report the results of parameter-free quasiparticle calculations of the single-particle excitation spectrum which show that CaB_6 is not a semimetal but a semiconductor with a band gap of 0.8 eV. Magnetism in La_xCa_{1-x}B_6 occurs just on the metallic side of a Mott transition in the La-induced impurity band.Comment: 4 pages, 1 postscript figur
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