Fast Mesh Refinement in Pseudospectral Optimal Control

Mesh refinement in pseudospectral (PS) optimal control is embarrassingly easy --- simply increase the order $N$ of the Lagrange interpolating polynomial and the mathematics of convergence automates the distribution of the grid points. Unfortunately, as $N$ increases, the condition number of the resulting linear algebra increases as $N^2$; hence, spectral efficiency and accuracy are lost in practice. In this paper, we advance Birkhoff interpolation concepts over an arbitrary grid to generate well-conditioned PS optimal control discretizations. We show that the condition number increases only as $\sqrt{N}$ in general, but is independent of $N$ for the special case of one of the boundary points being fixed. Hence, spectral accuracy and efficiency are maintained as $N$ increases. The effectiveness of the resulting fast mesh refinement strategy is demonstrated by using \underline{polynomials of over a thousandth order} to solve a low-thrust, long-duration orbit transfer problem.Comment: 27 pages, 12 figures, JGCD April 201

Enrichment exercises in spelling for grades two, three, and four

Thesis (Ed.M.)--Boston Universit

Time-trends and treatment gaps in the antithrombotic management of patients with atrial fibrillation after percutaneous coronary intervention: Insights from the CHUM AF-STENT Registry.

BACKGROUND: The management of atrial fibrillation and flutter (AF) patients undergoing percutaneous coronary intervention (PCI) has undergone a rapid recent evolution. In 2016, the Canadian Cardiovascular Society (CCS) published expert recommendations to help guide clinicians in balancing bleeding and thrombotic risks in these patients. HYPOTHESIS: Antithrombotic regimen prescriptions for AF patients undergoing PCI evolved after the publication of the 2016 CCS AF guidelines. METHODS: A prospective cohort of AF patients undergoing PCI with placement of a coronary stent from a single tertiary academic center was analyzed for the recommended antithrombotic regimen at discharge. Prescribing behavior was compared between three time periods (Cohort A [2010-2011]; Cohort B [2014-2015]; Cohort C [2017]) using the χ2 test. In addition, antithrombotic management in Cohorts B and C were compared to guideline-recommended therapy. RESULTS: A total of 459 patients with AF undergoing PCI were identified. Clinical and procedural characteristics were similar between cohorts, with the exception of an increase in drug-eluting stent (DES) use over time (P < .01). Overall, the rate of oral anticoagulation (OAC) increased over time (P < .01), associated with an increase in nonvitamin K OAC prescription (P < .01) and a concomitant decrease in vitamin K antagonist prescription (P < .01). Despite this, the overall rate of anticoagulation remains below what would be predicted with perfect guideline compliance (75% vs 94%, P < .01). CONCLUSION: There has been a dramatic shift in clinical practice for AF patients requiring PCI, with increases in prescription of OAC even in the context of an increase in the use of DES. However, room for further practice optimization still exists

What are the Marital Problems of Happy Couples? A Multimethod, Two‐Sample Investigation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162758/2/famp12483.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162758/1/famp12483_am.pd

Gain of Function Analysis Reveals Non-Redundant Roles for the Yersinia pestis Type III Secretion System Effectors YopJ, YopT, and YpkA [preprint]

Virulence of Yersinia pestis in mammals requires the type III secretion system, which delivers seven effector proteins into the cytoplasm of host cells to undermine immune responses. All seven of these effectors are conserved across Y. pestis strains, but three -- YopJ, YopT, and YpkA -- are apparently dispensable for virulence. Some degree of functional redundancy between effector proteins would explain both observations. Here, we use a combinatorial genetic approach to define the minimal subset of effectors required for full virulence in mice following subcutaneous infection. We found that a Y. pestis strain lacking YopJ, YopT, and YpkA is attenuated for virulence in mice, and that addition of any one of these effectors to this strain increases lethality significantly. YopJ, YopT, and YpkA likely contribute to virulence via distinct mechanisms. YopJ is uniquely able to cause macrophage cell death in vitro and to suppress accumulation of inflammatory cells to foci of bacterial growth in deep tissue, whereas YopT and YpkA cannot. The synthetic phenotypes that emerge when YopJ, YopT, and YpkA are removed in combination provide evidence that each enhances Y. pestis virulence, and that YopT and YpkA act through a mechanism distinct from that of YopJ

Separation and identification of dominant mechanisms in double photoionization

Double photoionization by a single photon is often discussed in terms of two contributing mechanisms, {\it knock-out} (two-step-one) and {\it shake-off} with the latter being a pure quantum effect. It is shown that a quasi-classical description of knock-out and a simple quantum calculation of shake-off provides a clear separation of the mechanisms and facilitates their calculation considerably. The relevance of each mechanism at different photon energies is quantified for helium. Photoionization ratios, integral and singly differential cross sections obtained by us are in excellent agreement with benchmark experimental data and recent theoretical results.Comment: 4 pages, 5 figure

Both Reintroduction and Recolonization Likely Contributed to the Re-establishment of a Fisher Population in East-central Alberta

Recently, Stewart et al. (2017) investigated the origins of contemporary fisher populations in the Cooking Lake Moraine (CLM) of east-central Alberta, Canada, where fishers (Pekania pennanti) from Ontario and Manitoba, Canada were reintroduced in the early 1990s. To address this objective, Stewart et al. (2017) compared microsatellite alleles from extant fisher populations in the CLM to those from Ontario, Manitoba, and other Alberta populations. They reported that the CLM population clustered with adjacent native Alberta populations, consistent with recolonization, but also that 2 of 109 microsatellite alleles in the CLM occurred only in the source populations from Ontario and Manitoba. Rather than allowing for the possibility that these alleles descended from reintroduced fishers, the authors speculated that they represented random mutations among fishers that recolonized the area naturally from nearby populations in Alberta, and concluded that the reintroduction had failed completely. We disagree with this conclusion for 2 reasons. We contend it is more likely that the 2 alleles represent a genetic signature from the individuals released during the reintroduction, rather than being the result of mutations. We further suggest that, irrespective of the genetic legacy of introduced fishers in the recovered population, the presence of reintroduced fishers in the CLM may have helped facilitate natural recolonization of the area by fishers from surrounding areas. In our view, Stewart et al.’s (2017) findings do not demonstrate conclusively that the reintroduction program failed; on the contrary, we argue that their findings indicate that reintroduced fishers likely contributed to the long-term persistence of fishers in the CLM. The uncertainty surrounding this case underscores the importance of genetic monitoring following reintroductions.https://digitalcommons.snc.edu/faculty_staff_works/1032/thumbnail.jp

Dynamic MAIT cell response with progressively enhanced innateness during acute HIV-1 infection.

Mucosa-associated invariant T (MAIT) cell loss in chronic HIV-1 infection is a significant insult to antimicrobial immune defenses. Here we investigate the response of MAIT cells during acute HIV-1 infection utilizing the RV217 cohort with paired longitudinal pre- and post-infection samples. MAIT cells are activated and expand in blood and mucosa coincident with peak HIV-1 viremia, in a manner associated with emerging microbial translocation. This is followed by a phase with elevated function as viral replication is controlled to a set-point level, and later by their functional decline at the onset of chronic infection. Interestingly, enhanced innate-like pathways and characteristics develop progressively in MAIT cells during infection, in parallel with TCR repertoire alterations. These findings delineate the dynamic MAIT cell response to acute HIV-1 infection, and show how the MAIT compartment initially responds and expands with enhanced function, followed by progressive reprogramming away from TCR-dependent antibacterial responses towards innate-like functionality