18 research outputs found

    Confinements regulate capillary instabilities of fluid threads

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    We study the breakup of confined fluid threads at low flow rates to understand instability mechanisms. To determine the critical conditions between the earlier quasi-stable necking stage and the later unstable collapse stage, simulations and experiments are designed to operate at an extremely low flow rate. Critical mean radii at neck centres are identified by the stop-flow method for elementary microfluidic configurations. Analytical investigations reveal two distinct origins of capillary instabilities. One is the gradient of capillary pressure induced by the confinements of geometry and external flow, whereas the other is the competition between local capillary pressure and internal pressure determined by the confinements

    Confinements regulate capillary instabilities of fluid threads

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    We study the breakup of confined fluid threads at low flow rates to understand instability mechanisms. To determine the critical conditions between the earlier quasi-stable necking stage and the later unstable collapse stage, simulations and experiments are designed to operate at an extremely low flow rate. Critical mean radii at neck centres are identified by the stop-flow method for elementary microfluidic configurations. Analytical investigations reveal two distinct origins of capillary instabilities. One is the gradient of capillary pressure induced by the confinements of geometry and external flow, whereas the other is the competition between local capillary pressure and internal pressure determined by the confinements

    Genome-wide linkage scan identifies two novel genetic loci for coronary artery disease: in GeneQuest families.

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    Coronary artery disease (CAD) is the leading cause of death worldwide. Recent genome-wide association studies (GWAS) identified >50 common variants associated with CAD or its complication myocardial infarction (MI), but collectively they account for <20% of heritability, generating a phenomena of "missing heritability". Rare variants with large effects may account for a large portion of missing heritability. Genome-wide linkage studies of large families and follow-up fine mapping and deep sequencing are particularly effective in identifying rare variants with large effects. Here we show results from a genome-wide linkage scan for CAD in multiplex GeneQuest families with early onset CAD and MI. Whole genome genotyping was carried out with 408 markers that span the human genome by every 10 cM and linkage analyses were performed using the affected relative pair analysis implemented in GENEHUNTER. Affected only nonparametric linkage (NPL) analysis identified two novel CAD loci with highly significant evidence of linkage on chromosome 3p25.1 (peak NPL  = 5.49) and 3q29 (NPL  = 6.84). We also identified four loci with suggestive linkage on 9q22.33, 9q34.11, 17p12, and 21q22.3 (NPL  = 3.18-4.07). These results identify novel loci for CAD and provide a framework for fine mapping and deep sequencing to identify new susceptibility genes and novel variants associated with risk of CAD

    Novel Genetic Loci for CAD Identified by GWLS in the GeneQuest Families.

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    a<p>Based on Marshfield Medical Genetics marker set 11.</p>b<p>Based on either UCSC Genome Browser database or Marshfield Medical Genetics marker set 11.</p><p>Note that a marker with a two-point or multipoint NPL score of >4.99 (<i>P</i><3×10<sup>−7</sup>) was considered to be linked to CAD highly significantly; A two-point or multipoint NPL score between 3.18 and 4.08 indicates suggestive linkage <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113935#pone.0113935-Kruglyak1" target="_blank">[38]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113935#pone.0113935-Kruglyak2" target="_blank">[53]</a>.</p><p>Novel Genetic Loci for CAD Identified by GWLS in the GeneQuest Families.</p
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