Heating and decoherence suppression using decoupling techniques

We study the application of decoupling techniques to the case of a damped vibrational mode of a chain of trapped ions, which can be used as a quantum bus in linear ion trap quantum computers. We show that vibrational heating could be efficiently suppressed using appropriate ``parity kicks''. We also show that vibrational decoherence can be suppressed by this decoupling procedure, even though this is generally more difficult because the rate at which the parity kicks have to applied increases with the effective bath temperature.Comment: 13 pages, 5 figures. Typos corrected, references adde

Random field sampling for a simplified model of melt-blowing considering turbulent velocity fluctuations

In melt-blowing very thin liquid fiber jets are spun due to high-velocity air streams. In literature there is a clear, unsolved discrepancy between the measured and computed jet attenuation. In this paper we will verify numerically that the turbulent velocity fluctuations causing a random aerodynamic drag on the fiber jets -- that has been neglected so far -- are the crucial effect to close this gap. For this purpose, we model the velocity fluctuations as vector Gaussian random fields on top of a k-epsilon turbulence description and develop an efficient sampling procedure. Taking advantage of the special covariance structure the effort of the sampling is linear in the discretization and makes the realization possible

A comparison of five surface mixed layer models with a year of observations in the North Atlantic

Five upper ocean mixed layer models driven by ERA-Interim surface forcing are compared with a year of hydrographic observations of the upper 1000 m, taken at the Porcupine Abyssal Plain observatory site using profiling gliders. All the models reproduce sea surface temperature (SST) fairly well, with annual mean warm biases of 0.11  ° C (PWP model), 0.24  ° C (GLS), 0.31  ° C (TKE), 0.91  ° C (KPP) and 0.36  ° C (OSMOSIS). The main exception is that the KPP model has summer SSTs which are higher than the observations by nearly 3 ° . Mixed layer salinity (MLS) is not reproduced well by the models and the biases are large enough to produce a non-trivial density bias in the Eastern North Atlantic Central Water which forms in this region in winter. All the models develop mixed layers which are too deep in winter, with average winter mixed layer depth (MLD) biases between 160 and 228 m. The high variability in winter MLD is reproduced more successfully by model estimates of the depth of active mixing and/or boundary layer depth than by model MLD based on water column properties. After the spring restratification event, biases in MLD are small and do not appear to be related to the preceding winter biases. There is a very clear relationship between MLD and local wind stress in all models and in the observations during spring and summer, with increased wind speeds leading to deepening mixed layers, but this relationship is not present during autumn and winter. We hypothesize that the deepening of the MLD in autumn is so strongly driven by the annual cycle in surface heat flux that the winds are less significant in the autumn. The surface heat flux drives a diurnal cycle in MLD and SST from March onwards, though this effect is much more significant in the models than in the observations. We are unable to identify one model as definitely better than the others. The only clear differences between the models are KPP’s inability to accurately reproduce summer SSTs, and the OSMOSIS model’s more accurate reproduction of MLS

Development and characterization of acellular porcine pulmonary valve scaffolds for tissue engineering.

Currently available replacement heart valves all have limitations. This study aimed to produce and characterize an acellular, biocompatible porcine pulmonary root conduit for reconstruction of the right ventricular outflow tract e.g. during Ross procedure. A process for the decellularization of porcine pulmonary roots was developed incorporating trypsin treatment of the adventitial surface of the scraped pulmonary artery and sequential treatment with: hypotonic Tris buffer (HTB; 10mM Tris pH 8.0, 0.1% (w/v) EDTA, 10KIU aprotinin), 0.1% (w/v) SDS in HTB, two cycles of DNase and RNase, and sterilisation with 0.1% (v/v) peracetic acid. Histology confirmed an absence of cells and retention of the gross histoarchitecture. Immunohistochemistry further confirmed cell removal and partial retention of the extra cellular matrix, but a loss of collagen type IV. DNA levels were reduced by more than 96 % throughout all regions of the acellular tissue and no functional genes were detected using PCR. Total collagen levels were retained but there was a significant loss of glycosaminoglycans following decellularization. The biomechanical, hydrodynamic and leaflet kinematics properties were minimally affected by the process. Both immunohistochemical labelling and antibody absorption assay confirmed a lack of α-gal epitopes in the acellular porcine pulmonary roots and in vitro biocompatibility studies indicated that acellular leaflets and pulmonary arteries were not cytotoxic. Overall the acellular porcine pulmonary roots have excellent potential for development of a tissue substitute for right ventricular out flow tract reconstruction e.g. during the Ross procedure

Sociocultural considerations in aging men's health: implications and recommendations for the clinician

http://dx.doi.org/10.1016/j.jomh.2009.07.00

Heterozygous Variants in KMT2E Cause a Spectrum of Neurodevelopmental Disorders and Epilepsy.

We delineate a KMT2E-related neurodevelopmental disorder on the basis of 38 individuals in 36 families. This study includes 31 distinct heterozygous variants in KMT2E (28 ascertained from Matchmaker Exchange and three previously reported), and four individuals with chromosome 7q22.2-22.23 microdeletions encompassing KMT2E (one previously reported). Almost all variants occurred de novo, and most were truncating. Most affected individuals with protein-truncating variants presented with mild intellectual disability. One-quarter of individuals met criteria for autism. Additional common features include macrocephaly, hypotonia, functional gastrointestinal abnormalities, and a subtle facial gestalt. Epilepsy was present in about one-fifth of individuals with truncating variants and was responsive to treatment with anti-epileptic medications in almost all. More than 70% of the individuals were male, and expressivity was variable by sex; epilepsy was more common in females and autism more common in males. The four individuals with microdeletions encompassing KMT2E generally presented similarly to those with truncating variants, but the degree of developmental delay was greater. The group of four individuals with missense variants in KMT2E presented with the most severe developmental delays. Epilepsy was present in all individuals with missense variants, often manifesting as treatment-resistant infantile epileptic encephalopathy. Microcephaly was also common in this group. Haploinsufficiency versus gain-of-function or dominant-negative effects specific to these missense variants in KMT2E might explain this divergence in phenotype, but requires independent validation. Disruptive variants in KMT2E are an under-recognized cause of neurodevelopmental abnormalities

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Nucleotide sequence analysis of Jembrana disease virus: a bovine lentivirus associated with an acute disease syndrome

The complete nucleotide sequence of the RNA genome of Jembrana disease virus (JDV), a lentivirus that causes an acute disease syndrome in Bali cattle (Bos javanicus), is reported. In addition to the gag, pol and env genes and flanking long terminal repeats (LTRs) that characterize all retroviruses, a number of accessory genes represented by small multiply spliced ORFs in the central and 3′-terminal regions of the genome, including tat and rev that are typical of lentiviruses, were identified. The genome of JDV was 7732 bp in length, 750 bp smaller than the genome of bovine immunodeficiency virus (BIV) strain BIV127. A striking feature of the genome was the many deletions relative to BIV127, the largest of which were 471 bp from the env gene and 157 bp from the U3 (promoter) region in the LTR. There were also several insertions of up to 33 bp in the JDV genome relative to BIV127 found in the env gene and small ORFs that overlap env. Other significant genomic differences between JDV and BIV127 included changes to cis-acting sequences throughout the genome such as promoter and enhancer sequences in the LTR, the trans-activation response region, splice sites and frameshift sequences; alterations to the gag precursor protein cleavage sites and thus the processed products; loss of the vpw and vpy ORFs; and amino acid changes in all coding regions. The significance of these changes is discussed in relation to the differences in pathogenicity between JDV and BIV

Genomic sequence analysis identifies Jembrana disease virus as a new bovine lentivirus

Jembrana disease virus, the cause of an acute, severe disease in Bali (Bos javanicus) cattle in Indonesia was recently identified as a retrovirus, and possibly a lentivirus. We have produced sequence data representing 598 bp of the pol gene, amplified by PCR from viral cDNA using broadly reactive universal primers for retroviruses and more specific genus-reactive primers for lentiviruses. When the sequence data were compared with that of known lentiviruses and other bovine retroviruses, the closest alignment was with bovine immunodeficiency-like lentivirus (BIV), showing 74% nucleotide sequence identity. This confirmed that JDV is a lentivirus and that it is distinguishable from BIV. The pathogenesis of Jembrana disease is most unusual for a lentivirus infection and differs markedly from that reported for BIV infection