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When a wave breaks, it produces bubbles whose sizes depend on the breaking severity. This paper attempts to estimate wave breaking dissipation through a passive acoustic method. Initially, regular waves were forced to break in a flume. The breaking energy loss (severity) and the underwater acoustic noise were recorded. Two kinds of thresholds, in terms of sound wave amplitude and the ratio of sound wave height to period, respectively, were used together to identify the sound waves generated by newly formed bubbles. The frequencies of these sound waves are connected with the bubble sizes. Thus, a relationship between the mean bubble radius and the breaking severity was established and found to be linear. This laboratory relationship was then applied to Lake George data to study the breaking dissipation rate across the spectrum. An average acoustic spectral density threshold was proposed to identify breaking events from acoustic records in the field. The sound waves associated with bubble formation were selected by means of the same two kinds of threshold as used in the laboratory. Thus, the mean bubble radius of each breaking event was obtained and translated into the breaking severity. The values of experimental dissipation were compared with previous relevant results obtained through different methods as well as the wave breaking dissipation source terms ST6 (WAVEWATCH-III model) and are in good agreement with both of them.

Diseases that affect the regulation of bone turnover can lead to skeletal fragility and increased fracture risk. Members of the TGF-β superfamily have been shown to be involved in the regulation of bone mass. Activin A, a TGF-β signaling ligand, is present at high levels in bone and may play a role in the regulation of bone metabolism. Here we demonstrate that pharmacological blockade of ligand signaling through the high affinity receptor for activin, type II activin receptor (ActRIIA), by administration of the soluble extracellular domain of ActRIIA fused to a murine IgG2a-Fc, increases bone formation, bone mass, and bone strength in normal mice and in ovariectomized mice with established bone loss. These observations support the development of this pharmacological strategy for the treatment of diseases with skeletal fragility.

This paper describes the synthesis of two beta-phosphorylamide ligands and their coordination chemistry with the Ln ions Tb3+, Eu3+, and Sm3+. Both the ligands and Ln complexes were characterized by IR, NMR, MS, and X-ray crystallography. The luminescence properties of the Tb3+ and Eu3+ complexes were also characterized, including the acquisition of lifetime decay curves. In the solid state, the Tb3+ and Sm3+ ligand complexes were found to have a 2:2 stoichiometry when analyzed by X-ray diffraction. In these structures, the Ln ion was bound by both oxygen atoms of each beta-phosphorylamide moiety of the ligands. The Tb3+ and Eu3+ complexes were modestly emissive as solutions in acetonitrile, with lifetime values that fell within typical ranges.

OBJECTIVE To assess the burden of bloodstream infections (BSIs) among pediatric hematology-oncology (PHO) inpatients, to propose a comprehensive, all-BSI tracking approach, and to discuss how such an approach helps better inform within-center and across-center differences in CLABSI rate DESIGN Prospective cohort study SETTING US multicenter, quality-improvement, BSI prevention network PARTICIPANTS PHO centers across the United States who agreed to follow a standardized central-line-maintenance care bundle and track all BSI events and central-line days every month. METHODS Infections were categorized as CLABSI (stratified by mucosal barrier injury-related, laboratory-confirmed BSI [MBI-LCBI] versus non-MBI-LCBI) and secondary BSI, using National Healthcare Safety Network (NHSN) definitions. Single positive blood cultures (SPBCs) with NHSN defined common commensals were also tracked. RESULTS Between 2013 and 2015, 34 PHO centers reported 1,110 BSIs. Among them, 708 (63.8%) were CLABSIs, 170 (15.3%) were secondary BSIs, and 232 (20.9%) were SPBCs. Most SPBCs (75%) occurred in patients with profound neutropenia; 22% of SPBCs were viridans group streptococci. Among the CLABSIs, 51% were MBI-LCBI. Excluding SPBCs, CLABSI rates were higher (88% vs 77%) and secondary BSI rates were lower (12% vs 23%) after the NHSN updated the definition of secondary BSI (P<.001). Preliminary analyses showed across-center differences in CLABSI versus secondary BSI and between SPBC and CLABSI versus non-CLABSI rates. CONCLUSIONS Tracking all BSIs, not just CLABSIs in PHO patients, is a patient-centered, clinically relevant approach that could help better assess across-center and within-center differences in infection rates, including CLABSI. This approach enables informed decision making by healthcare providers, payors, and the public. Infect Control Hosp Epidemiol 2017;38:690-696.

Until recently, the degradation of aberrant and unassembled proteins retained in the endoplasmic reticulum (ER) was thought to involve unidentified ER-localized proteases. We now show that the ER-associated degradation (ERAD) of two mutant proteins that accumulate in the ER lumen is inhibited in a proteasome-defective yeast strain and when cytosol from this mutant is used in an in vitro assay. In addition, ERAD is limited in vitro in the presence of the proteasome inhibitors, 3,4-dichloroisocoumarin and lactacystin. Furthermore, we find that an ERAD substrate is exported from ER-derived microsomes, and the accumulation of exported substrate is 2-fold greater when proteasome mutant cytosol is used in place of wild-type cytosol. We conclude that lumenal ERAD substrates are exported from the yeast ER to the cytoplasm for degradation by the proteasome complex

Recent advances in a technique to identify and catalog waves that ride on larger-scale carrier waves are described in detail. The latest developments allow the riding wave removal technique to correctly identify and replace riding waves at the Nyquist frequency scale. Examples of the technique are provided for two diverse datasets: the Black Sea and Lake George. A sample of the riding wave characteristics extracted using this method is presented.

The APS, SH2-B and LNK proteins are adapters that activate and modulate receptor tyrosine kinase and JAK/STAT signaling. We now show that a conserved N-terminal domain mediates APS homodimerization. We determined the crystal structure of the dimerization domain at a resolution of 1.7 Å using bromide ion MAD phasing. Each molecule contributes two helices to a compact four-helix bundle having a bisecting-U topology. Its most conspicuous feature is a stack of interdigitated phenylalanine side chains at the domain core. These residues create a new motif we refer to as a 'phenylalanine zipper,' which is critical to dimerization. A newly developed bridging yeast tri-hybrid assay showed that APS dimerizes JAK2, insulin receptor and IGF1 receptor kinases using its SH2 and dimerization domains. Dimerization via the phenylalanine zipper domain provides a mechanism for activating and modulating tyrosine kinase activity even in the absence of extracellular ligands.

Neonatal hematology is a fast-growing field, and hematologic problems occur in the majority of sick neonates. Focusing on clinical issues and problem-solving, this is a fully revised and updated revision of a successful practical guide to the pathogenesis, recognition and management of hematologic problems in the neonate. The second edition begins with chapters on the history of neonatal hematology, hematopoiesis, and the immunologic system. Subsequent sections are devoted to erythrocyte disorders, platelet disorders, leucocyte disorders, immunologic disorders and hemostatic disorders. New to this edition are an expanded coverage of neonatal oncology, cord blood utilization, neonatal screening, prenatal diagnosis and hyperbilirubinemia. Written by practising physicians specializing in pediatric hematology, neonatology, immunology, pediatric infectious disease and transfusion medicine, this is an essential text for pediatric hematologists, NICU specialists, neonatologists and neonatal nurse practitioners.

BackgroundPrevious studies have shown that differential exposure to lifestyle factors may mediate the association between education and coronary heart diseases (CHD). However, few studies have examined the potential roles of allostatic load (AL) or differential susceptibility.Methods25 310 men and 26 018 women aged 35–74 and CHD free at baseline were identified from 21 European cohorts and followed for a median of 10 years, to investigate the mediating role of AL, as well as of smoking, alcohol use and body mass index (BMI), on educational differences in CHD incidence, applying marginal structural models and three-way decomposition.ResultsAL is a mediator of the association between educational status and CHD incidence, with the highest proportion mediated observed among women and largely attributable to differential exposure, (28% (95% CI 19% to 44%)), with 8% (95% CI 0% to 16%) attributable to differential susceptibility. The mediating effects of smoking, alcohol and BMI, compared with AL, were relatively small for both men and women.ConclusionOverall, the educational inequalities in CHD incidence were partially mediated through differential exposure to AL. By contrast, the mediation of the educational gradient in CHD by investigated lifestyle risk factors was limited. As differential susceptibility in men was found to have a predominant role in the accumulation of AL in low educational classes, the investigation of AL-related risk factors is warranted.

Three authors present very different views of the developing field of systems biology. Keep it simple Uri Alon's book An Introduction to Systems Biology: Design Principles of Biological Circuits , has done much to introduce systems biology to a wider audience. It's one of a clutch of systems biology texts reviewed this week. And in Connections, Alon reflects on the idea that the apparent complexity of biological systems is just that, apparent. A closer look suggests that biological net works display a degree of simplicity that is intriguing given that cells evolved to survive, and not for scientists to understand.