1,236 research outputs found

    Wafer-level packaged RF-MEMS switches fabricated in a CMOS fab

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    Reports on wafer-level packaged RF-MEMS switches fabricated in a commercial CMOS fab. Switch fabrication is based on a metal surface micromachining process. A novel wafer-level packaging scheme is developed, whereby the switches are housed in on-chip sealed cavities using benzocyclobutene (BCB) as the bonding and sealing material. Measurements show that the influence of the wafer-level package on the RF performance can be made very small.\ud \u

    DNA Damage Response and Mismatch Repair Gene Defects in Advanced and Metastatic Prostate Cancer.

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    Alterations in DNA damage response (DDR) and related genes are present in up to 25% of advanced prostate cancers (PCa). Most frequently altered genes are involved in the homologous recombination repair, the Fanconi anemia, and the mismatch repair pathways, and their deficiencies lead to a highly heterogeneous spectrum of DDR-deficient phenotypes. More than half of these alterations concern non-BRCA DDR genes. From a therapeutic perspective, poly-ADP-ribose polymerase inhibitors have demonstrated robust clinical efficacy in tumors with BRCA2 and BRCA1 alterations. Mismatch repair-deficient PCa, and a subset of CDK12-deficient PCa, are vulnerable to immune checkpoint inhibitors. Emerging data point to the efficacy of ATR inhibitors in PCa with ATM deficiencies. Still, therapeutic implications are insufficiently clarified for most of the non-BRCA DDR alterations, and no successful targeted treatment options have been established

    Modelling the evolution of distributions : an application to major league baseball

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    We develop Bayesian techniques for modelling the evolution of entire distributions over time and apply them to the distribution of team performance in Major League baseball for the period 1901-2000. Such models offer insight into many key issues (e.g. competitive balance) in a way that regression-based models cannot. The models involve discretizing the distribution and then modelling the evolution of the bins over time through transition probability matrices. We allow for these matrices to vary over time and across teams. We find that, with one exception, the transition probability matrices (and, hence, competitive balance) have been remarkably constant across time and over teams. The one exception is the Yankees, who have outperformed all other teams

    Universal cloning of continuous quantum variables

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    The cloning of quantum variables with continuous spectra is analyzed. A universal - or Gaussian - quantum cloning machine is exhibited that copies equally well the states of two conjugate variables such as position and momentum. It also duplicates all coherent states with a fidelity of 2/3. More generally, the copies are shown to obey a no-cloning Heisenberg-like uncertainty relation.Comment: 4 pages, RevTex. Minor revisions, added explicit cloning transformation, added reference

    Emergence of Anti-Cancer Drug Resistance: Exploring the Importance of the Microenvironmental Niche via a Spatial Model

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    Practically, all chemotherapeutic agents lead to drug resistance. Clinically, it is a challenge to determine whether resistance arises prior to, or as a result of, cancer therapy. Further, a number of different intracellular and microenvironmental factors have been correlated with the emergence of drug resistance. With the goal of better understanding drug resistance and its connection with the tumor microenvironment, we have developed a hybrid discrete-continuous mathematical model. In this model, cancer cells described through a particle-spring approach respond to dynamically changing oxygen and DNA damaging drug concentrations described through partial differential equations. We thoroughly explored the behavior of our self-calibrated model under the following common conditions: a fixed layout of the vasculature, an identical initial configuration of cancer cells, the same mechanism of drug action, and one mechanism of cellular response to the drug. We considered one set of simulations in which drug resistance existed prior to the start of treatment, and another set in which drug resistance is acquired in response to treatment. This allows us to compare how both kinds of resistance influence the spatial and temporal dynamics of the developing tumor, and its clonal diversity. We show that both pre-existing and acquired resistance can give rise to three biologically distinct parameter regimes: successful tumor eradication, reduced effectiveness of drug during the course of treatment (resistance), and complete treatment failure
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