204 research outputs found

    Minimizing Error Rate in the Updation of Physicians’ Profile

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    The Provider Update Management is the project undertaken by iSpace Global Services Company. MultiPlan is the leading provider of independent national Payer and Provider Organizations (PPO) networks and related cost management services. It was founded in 1980 as a New York hospital network. With more than half a million healthcare providers under contract, an estimated 40 million consumers access the network products. About 65 million claims are processed through the network each year. The Company desired to understand the process of updating the Provider data without any errors committed by the users. The company believes that the SIX SIGMA methodology is the most useful methodology to understand the root cause and take the improvement steps to sustain the Benchmark in Quality. This study focuses on achieving internal and external quality targets by minimizing error incidence in the updating process of physicians’ data through systematic deployment of Six Sigma DMAIC methodology resulting in substantial improvement of the process quality

    Current Contour Based Design Methodology for IMN Design of Doherty Power Amplifiers

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    Carrier aggregation (CA) is used in modern communication schemes to increase com- munication bandwidth (BW) and reduce redundant equipment. This combined with the already high peak to average power ratio (PAPR) signals in use for complex modulation schemes results in stringent linearity requirements and degradation in the average drain efficiency (DE) in basic power amplifier (PA) topologies. This has led to research interests in highly efficient broadband PAs capable of addressing the bandwidth and multi-standard requirements. Several techniques have been developed to enhance the efficiency of PAs when driven by a modulated signal with high PAPR, but amongst them the Doherty power amplifier (DPA) has garnered considerable attention in research and commercial adoption. In this work the importance of the current profiles at the drain of the main and peaking amplifier in the DPA is examined. By looking at the effect of the nonlinear capacitance at the input of the transistor, it is seen that choice of impedance presented at the fundamental and second harmonic have a drastic effect on the performance of the overall PA. To combat these issues, the constant current circle is introduced to aid in the design of the input matching network (IMN) of the main and peaking. By using the current contours the fundamental drain current can be carefully dictated by presenting the correct impedance at the gate of the transistor versus frequency and input drive. Using the current contours in conjunction with the design methodology outlined allows for the simple design of DPA IMN to extract the most performance out of the output combining node (OCN). To validate the introduced material a 12-W 3.0-5.0GHz DPA was constructed using GaN HEMT transistors. The simulation results showed that the current profiles remained within range when using an iterative design approach along with current contours. Measurement results showed that the PA was able to achieve a gain of 8dB within the designed band. As well the efficiency at both peak and BO was greater than 37% across the band. To show the performance of the PA under modulated signal, the PA was tested with a 80MHz intra- band non-contguous signal at 3.3GHz. Before DPD the reported ACLR was 37dBc/Hz. Applying a DPD engine, the ACLR was brought down to 48dBc/Hz, or the noise floor of the equipment

    Active colloids in complex fluids

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    We review recent work on active colloids or swimmers, such as self-propelled microorganisms, phoretic colloidal particles, and artificial micro-robotic systems, moving in fluid-like environments. These environments can be water-like and Newtonian but can frequently contain macromolecules, flexible polymers, soft cells, or hard particles, which impart complex, nonlinear rheological features to the fluid. While significant progress has been made on understanding how active colloids move and interact in Newtonian fluids, little is known on how active colloids behave in complex and non-Newtonian fluids. An emerging literature is starting to show how fluid rheology can dramatically change the gaits and speeds of individual swimmers. Simultaneously, a moving swimmer induces time dependent, three dimensional fluid flows, that can modify the medium (fluid) rheological properties. This two-way, non-linear coupling at microscopic scales has profound implications at meso- and macro-scales: steady state suspension properties, emergent collective behavior, and transport of passive tracer particles. Recent exciting theoretical results and current debate on quantifying these complex active fluids highlight the need for conceptually simple experiments to guide our understanding.Comment: 6 figure

    Micromechanical Behaviour in Shearing of Reproduced Flat LBS Grains with Strong and Weak Artificial Bonds

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    The shearing behaviour of reproduced flat LBS grains artificially bonded with ordinary Portland cement (OPC) and plaster of Paris (PP) was examined using micromechanical experiments. Monotonic shearing tests showed a distinct variation in the load–displacement relationship at low, medium and high normal loads, and a nonlinear shear strength envelope was proposed. For OPC-bonded sand grains, a brittle–ductile transition at 20–30 N normal load was observed and three breakage mechanisms in shearing (chipping, shear cracks and crushing) were distinguished in accordance with the changes in the load–displacement curves. OPC-bonded sands showed a predominant dilation at lower normal loads, whereas PP-bonded sands were highly compressive. Based on previously published works using element-scale tests, a new mechanism for dilation under micromechanical testing was proposed in the study. Cyclic shearing tests were conducted on OPC-bonded sands, and the effects of increased displacement amplitude and normal load were highlighted

    Planar broadband antenna for 2G/3G systems

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    A planar antenna with broadband gestalt is presented for mobile networks. The structure of the antenna is made up of a folded dipole pair with an L-figure microstrip coupling line. The microstrip coupling along with the dipoles are attached on a similar substrate. The radiation parts are plotted at 1.7 GHz, 2.2 GHz, and 2.7 GHz. A flexible coaxial cable made of perfect electric conductor (PEC) material is attached to the L-figure microstrip whereas the outside conductor made up of RO4350B material is attached to the coplanar strip of line. The gain of the antenna is almost 9 dBi. The benefit of the planar structure is that it offers a simple feeding structure and compact size that is necessary for second generation (2G)/third-generation (3G)/long-term evolution (LTE) systems. Finally, the antenna proposed is designed by using computer simulation technology (CST) microwave studio

    Emergence of compensatory mutations reveals the importance of electrostatic interactions between HIV-1 integrase and genomic RNA

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    HIV-1 integrase (IN) has a noncatalytic function in virion maturation through its binding to the viral RNA genome (gRNA). Class II IN substitutions inhibit IN-gRNA binding and result in the formation of virions with aberrant morphologies marked by mislocalization of the gRNA between the capsid lattice and the lipid envelope. These viruses are noninfectious due to a block at an early reverse transcription stage in target cells. HIV-1 IN utilizes basic residues within its C-terminal domain (CTD) to bind to the gRNA; however, the molecular nature of how these residues mediate gRNA binding and whether other regions of IN are involved remain unknown. To address this, we have isolated compensatory substitutions in the background of a class II IN mutant virus bearing R269A/K273A substitutions within the IN-CTD. We found that the nearby D256N and D270N compensatory substitutions restored the ability of IN to bind gRNA and led to the formation of mature infectious virions. Reinstating the local positive charge of the IN-CTD through individual D256R, D256K, D278R, and D279R substitutions was sufficient to specifically restore IN-gRNA binding and reverse transcription for the IN R269A/K273A as well as the IN R262A/R263A class II mutants. Structural modeling suggested that compensatory substitutions in the D256 residue created an additional interaction interface for gRNA binding, whereas other substitutions acted locally within the unstructured C-terminal tail of IN. Taken together, our findings highlight the essential role of CTD in gRNA binding and reveal the importance of pliable electrostatic interactions between the IN-CTD and the gRNA

    Genome-wide analysis of heterogeneous nuclear ribonucleoprotein (hnRNP) binding to HIV-1 RNA reveals a key role for hnRNP H1 in alternative viral mRNA splicing

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    Alternative splicing of HIV-1 mRNAs increases viral coding potential and controls the levels and timing of gene expression. HIV-1 splicing is regulated in part by heterogeneous nuclear ribonucleoproteins (hnRNPs) and their viral target sequences, which typically repress splicing when studied outside their native viral context. Here, we determined the location and extent of hnRNP binding to HIV-1 mRNAs and their impact on splicing in a native viral context. Notably, hnRNP A1, hnRNP A2, and hnRNP B1 bound to many dispersed sites across viral mRNAs. Conversely, hnRNP H1 bound to a few discrete purine-rich sequences, a finding that was mirrore

    Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell

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    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) variants govern transmissibility, responsiveness to vaccination, and disease severity. In a screen for new models of SARS-CoV-2 infection, we identify human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of angiotensin-converting enzyme 2 (ACE2) expression. Remarkably, H522 infection requires the E484D S variant; viruses expressing wild-type S are not infectious. Anti-S monoclonal antibodies differentially neutralize SARS-CoV-2 E484D S in H522 cells as compared to ACE2-expressing cells. Sera from vaccinated individuals block this alternative entry mechanism, whereas convalescent sera are less effective. Although the H522 receptor remains unknown, depletion of surface heparan sulfates block H522 infection. Temporally resolved transcriptomic and proteomic profiling reveal alterations in cell cycle and the antiviral host cell response, including MDA5-dependent activation of type I interferon signaling. These findings establish an alternative SARS-CoV-2 host cell receptor for the E484D SARS-CoV-2 variant, which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis

    Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell

    Get PDF
    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) variants govern transmissibility, responsiveness to vaccination, and disease severity. In a screen for new models of SARS-CoV-2 infection, we identify human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of angiotensin-converting enzyme 2 (ACE2) expression. Remarkably, H522 infection requires the E484D S variant; viruses expressing wild-type S are not infectious. Anti-S monoclonal antibodies differentially neutralize SARS-CoV-2 E484D S in H522 cells as compared to ACE2-expressing cells. Sera from vaccinated individuals block this alternative entry mechanism, whereas convalescent sera are less effective. Although the H522 receptor remains unknown, depletion of surface heparan sulfates block H522 infection. Temporally resolved transcriptomic and proteomic profiling reveal alterations in cell cycle and the antiviral host cell response, including MDA5-dependent activation of type I interferon signaling. These findings establish an alternative SARS-CoV-2 host cell receptor for the E484D SARS-CoV-2 variant, which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis
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