Dependence of shock-tube boundary layers on shock strength

Using familiar considerations of vorticity transport, the essential behavior of shock-tube boundary layers is explicitly exhibited; the nearly constant functions that cannot be calculated analytically are evaluated numerically and compared with Mirels' correlations

Development and myogenesis of the vermiform Buddenbrockia (Myxozoa) and implications for cnidarian body plan evolution

email ORCID ID© 2012 Gruhl and Okamura; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The attached file is the published version of the article.© 2012 Gruhl and Okamura; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The attached file is the published version of the article

Observations and models for needle-tissue interactions

The asymmetry of a bevel-tip needle results in the needle naturally bending when it is inserted into soft tissue. In this study we present a mechanics-based model that calculates the deflection of the needle embedded in an elastic medium. Microscopic observations for several needle- gel interactions were used to characterize the interactions at the bevel tip and along the needle shaft. The model design was guided by microscopic observations of several needle- gel interactions. The energy-based model formulation incor- porates tissue-specific parameters such as rupture toughness, nonlinear material elasticity, and interaction stiffness, and needle geometric and material properties. Simulation results follow similar trends (deflection and radius of curvature) to those observed in macroscopic experimental studies of a robot- driven needle interacting with different kinds of gels. These results contribute to a mechanics-based model of robotic needle steering, extending previous work on kinematic models

Characterisation of polymorphic microsatellite loci for the bryozoan Fredericella sultana, the primary host of the causative agent of salmonid proliferative kidney disease

0000-0001-7279-715X© Springer Science+Business Media Dordrecht 2014. The attached document is the authors' final accepted version of the journal article. You are advised to consult the publisher's version if you wish to cite from it

First microsatellite loci of the myxozoan parasite Tetracapsuloides bryosalmonae, the causative agent of proliferative kidney disease (PKD)

0000-0001-7279-715XCopyright © 2015 Inter-Research. The attached document is the authors' final accepted/submitted version of the journal article. You are advised to consult the publisher's version if you wish to cite from it

Newcomers Meet the Intracluster Medium in the Coma Cluster

A main topic at this meeting is how galaxies are affected when they enter for the first time the cluster environment from the outskirts. Most of the times we are forced to infer the environmental effects indirectly, relying on systematic variations of galaxy properties with environment, but there aren't many examples of direct observations able to unveil ongoing transformations taking place, and the corresponding mechanism producing it. We present a case in which it is possible to identify the cluster environment, and in particular the intracluster medium and the recent infall history of galaxies onto the cluster, as the cause for a recent, abrupt change in the evolutionary history of galaxies.Comment: 5 pages, 1 postscript figure -- to appear in "Outskirts of Galaxy Clusters: intense life in the suburbs", IAU Colloquium N. 195, 2004, ed. A Diaferi

New Improved Photometric Redshifts of Galaxies in the HDF

We report new improved photometric redshifts of 1048 galaxies in the Hubble Deep Field (HDF). A standard chi^2 minimizing method is applied to seven-color UBVIJHK photometry by Fernandez-Soto, Lanzetta, & Yahil (1999). We use 187 template SEDs representing a wide variety of morphology and age of observed galaxies based on a population synthesis model by Kodama & Arimoto (1997). We introduce two new recipes. First, the amount of the internal absorption is changed as a free parameter in the range of E(B-V)=0.0 to 0.5 with an interval of 0.1. Second, the absorption due to intergalactic HI clouds is also changed by a factor of 0.5, 1.0, and 1.5 around the opacity given by Madau (1995). The total number of template SEDs is thus 187x6x3=3,366, except for the redshift grid. The dispersion sigma_z of our photometric redshifts with respect to spectroscopic redshifts is sigma_z=0.08 and 0.24 for z2, respectively, which are smaller than the corresponding values (sigma_z=0.09 and 0.45) by Fernandez-Soto et al. Improvement is significant, especially in z>2. This is due to smaller systematic errors which are largely reduced mainly by including three opacities due to intergalactic HI clouds. We discuss redshift distribution N(z) and cosmic star formation rate based on our new photometric redshifts.Comment: 24 pages including 16 eps figures; accepted for publication in Ap

Clinical correlates of blood-derived circulating tumor DNA in pancreatic cancer.

BackgroundTreatment outcomes for patients with advanced pancreatic ductal adenocarcinoma (PDAC) remain dismal. There are unmet needs for understanding the biologic basis of this malignancy using novel next-generation sequencing technologies. Herein, we investigated the clinical utility of circulating tumor DNA (ctDNA) (the liquid biopsy) in this malignancy.MethodsctDNA was analyzed in 112 patients with PDAC (54-73 genes) and tissue DNA in 66 patients (315 genes) (both clinical-grade next-generation sequencing). Number of alterations, %ctDNA, concordance between ctDNA and tissue DNA, and correlation of ctDNA results with survival were assessed.ResultsThe most common genes altered in ctDNA were TP53 (46% of patients, N = 51) and KRAS (44%, N = 49). Median number of characterized ctDNA alterations per patient was 1 (range, 0-6), but patients with advanced PDAC had significantly higher numbers of ctDNA alterations than those with surgically resectable disease (median, 2 versus 0.5, P = 0.04). Overall, 75% (70/94) of advanced tumors had ≥ 1 ctDNA alteration. Concordance rate between ctDNA and tissue DNA alterations was 61% for TP53 and 52% for KRAS. Concordance for KRAS alterations between ctDNA and tissue DNA from metastatic sites was significantly higher than between ctDNA and primary tumor DNA (72% vs 39%, P = 0.01). Importantly, higher levels of total %ctDNA were an independent prognostic factor for worse survival (hazard ratio, 4.35; 95% confidence interval, 1.85-10.24 [multivariate, P = 0.001]). A patient with three ctDNA alterations affecting the MEK pathway (GNAS, KRAS, and NF1) attained a response to trametinib monotherapy ongoing at 6 months.ConclusionsOur findings showed that ctDNA often harbored unique alterations some of which may be targetable and that significantly greater numbers of ctDNA alterations occur in advanced versus resectable disease. Furthermore, higher ctDNA levels were a poor prognostic factor for survival

Revisiting Epidermal Growth Factor Receptor (EGFR) Amplification as a Target for Anti-EGFR Therapy: Analysis of Cell-Free Circulating Tumor DNA in Patients With Advanced Malignancies.

PurposeTo date, evidence for tissue epidermal growth factor receptor (EGFR) overexpression as a biomarker for anti-EGFR therapies has been weak. We investigated the genomic landscape of EGFR amplification in blood-derived cell-free tumor DNA (cfDNA) across diverse cancers and the role of anti-EGFR therapies in achieving response.MethodsWe assessed EGFR amplification status among 28,584 patients with malignancies evaluated by clinical-grade next-generation sequencing (NGS) of blood-derived cfDNA (54- to 73-gene panel). Furthermore, we curated the clinical characteristics of 1,434 patients at the University of California San Diego who had cfDNA testing by this NGS test.ResultsOverall, EGFR amplification was detected in cfDNA from 8.5% of patients (2,423 of 28,584), most commonly in colorectal (16.3% [458 of 2,807]), non-small-cell lung (9.0% [1,096 of 12,197]), and genitourinary cancers (8.1% [170 of 2,104]). Most patients had genomic coalterations (96.9% [95 of 98]), frequently involving genes affecting other tyrosine kinases (72.4% [71 of 98]), mitogen-activated protein kinase cascades (56.1% [55 of 98]), cell-cycle-associated signals (52.0% [51 of 98]), and the phosphoinositide 3-kinase pathway (35.7% [35 of 98]). EGFR amplification emerged in serial cfDNA after various anticancer therapies (n = 6), including checkpoint inhibitors (n = 4), suggesting a possible role for these amplifications in acquired resistance. Nine evaluable patients with EGFR amplification were treated with anti-EGFR-based regimens; five (55.6%) achieved partial responses, including three patients whose tissue NGS lacked EGFR amplification.ConclusionEGFR amplification was detected in cfDNA among 8.5% of 28,584 diverse cancers. Most patients had coexisting alterations. Responses were observed in five of nine patients who received EGFR inhibitors. Incorporating EGFR inhibitors into the treatment regimens of patients harboring EGFR amplification in cfDNA merits additional study