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Search Results: 1 - 10 of 194363 matches for " Joshua D. MacArthur "
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Hamilton-Jacobi Theory and Moving Frames
Joshua D. MacArthur,Raymond G. McLenaghan,Roman G. Smirnov
Symmetry, Integrability and Geometry : Methods and Applications , 2007,
Abstract: The interplay between the Hamilton-Jacobi theory of orthogonal separation of variables and the theory of group actions is investigated based on concrete examples.
Hamilton-Jacobi Theory and Moving Frames
Joshua D. MacArthur,Raymond G. McLenaghan,Roman G. Smirnov
Physics , 2007, DOI: 10.3842/SIGMA.2007.070
Abstract: The interplay between the Hamilton-Jacobi theory of orthogonal separation of variables and the theory of group actions is investigated based on concrete examples.
Profile of etravirine for the treatment of HIV infection
Alice Tseng, Rodger D MacArthur
Therapeutics and Clinical Risk Management , 2010, DOI: http://dx.doi.org/10.2147/TCRM.S3128
Abstract: ofile of etravirine for the treatment of HIV infection Review (4360) Total Article Views Authors: Alice Tseng, Rodger D MacArthur Published Date January 2010 Volume 2010:6 Pages 49 - 58 DOI: http://dx.doi.org/10.2147/TCRM.S3128 Alice Tseng1, Rodger D MacArthur2 1Toronto General Hospital, Toronto, ON, Canada; 2Division of Infectious Diseases, Wayne State University, Detroit, Michigan, USA Abstract: Etravirine is a second-generation non-nucleoside reverse transcriptase inhibitor (NNRTI) with the advantages of in vitro potency against many strains of virus resistant to efavirenz and nevirapine, as well as a higher genetic barrier to resistance. Etravirine is indicated for use in treatment-experienced patients, and the approved dose in adults is 200 mg twice daily. Etravirine should be administered after a meal as bioavailability is significantly reduced when taken in the fasting state. Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19. Etravirine may be coadministered with nucleoside/tide reverse transcriptase inhibitors, raltegravir and boosted darunavir, lopinavir, and saquinavir without dosage adjustment. Etravirine should not be given with other NNRTIs, unboosted protease inhibitors, and atazanavir/ritonavir, tipranavir/ritonavir, and fosamprenavir/ritonavir due to unfavorable drug interactions. In randomized, controlled trials, twice daily etravirine combined with darunavir/ritonavir plus optimized background therapy demonstrated better efficacy compared to darunavir/ritonavir plus optimized background therapy alone in treatment experienced populations out to 96 weeks follow-up. The main etravirine-associated toxicity is mild to moderate self-limiting rash, although severe and sometimes fatal hypersensitivity reactions have been reported. Etravirine offers a potent sequencing option after the development of resistance to first-line NNRTIs, and is a welcome addition to this established drug class.
Profile of etravirine for the treatment of HIV infection
Alice Tseng,Rodger D MacArthur
Therapeutics and Clinical Risk Management , 2010,
Abstract: Alice Tseng1, Rodger D MacArthur21Toronto General Hospital, Toronto, ON, Canada; 2Division of Infectious Diseases, Wayne State University, Detroit, Michigan, USAAbstract: Etravirine is a second-generation non-nucleoside reverse transcriptase inhibitor (NNRTI) with the advantages of in vitro potency against many strains of virus resistant to efavirenz and nevirapine, as well as a higher genetic barrier to resistance. Etravirine is indicated for use in treatment-experienced patients, and the approved dose in adults is 200 mg twice daily. Etravirine should be administered after a meal as bioavailability is significantly reduced when taken in the fasting state. Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19. Etravirine may be coadministered with nucleoside/tide reverse transcriptase inhibitors, raltegravir and boosted darunavir, lopinavir, and saquinavir without dosage adjustment. Etravirine should not be given with other NNRTIs, unboosted protease inhibitors, and atazanavir/ritonavir, tipranavir/ritonavir, and fosamprenavir/ritonavir due to unfavorable drug interactions. In randomized, controlled trials, twice daily etravirine combined with darunavir/ritonavir plus optimized background therapy demonstrated better efficacy compared to darunavir/ritonavir plus optimized background therapy alone in treatment experienced populations out to 96 weeks follow-up. The main etravirine-associated toxicity is mild to moderate self-limiting rash, although severe and sometimes fatal hypersensitivity reactions have been reported. Etravirine offers a potent sequencing option after the development of resistance to first-line NNRTIs, and is a welcome addition to this established drug class.Keywords: etravirine, review, efficacy, resistance, pharmacology
Symmetry and Self-Organization in Complex Systems
B. D. MacArthur,J. W. Anderson
Physics , 2006,
Abstract: We show that, in contrast to classical random graph models, many real-world complex systems -- including a variety of biological regulatory networks and technological networks such as the internet -- spontaneously self-organize to a richly symmetric state. We consider the organizational origins of symmetry and find that growth with preferential attachment confers symmetry in highly branched networks. We deconstruct the automorphism group of some real-world networks and find that some, but not all, real-world symmetry can be accounted for by branching. We also uncover an intriguing correspondence between the size of the automorphism group of growing random trees and the random Fibonacci sequences.
An Approach to Parallel Simulation of Ordinary Differential Equations  [PDF]
Joshua D. Carl, Gautam Biswas
Journal of Software Engineering and Applications (JSEA) , 2016, DOI: 10.4236/jsea.2016.95019
Abstract: Cyber-physical systems (CPS) represent a class of complex engineered systems where functionality and behavior emerge through the interaction between the computational and physical domains. Simulation provides design engineers with quick and accurate feedback on the behaviors generated by their designs. However, as systems become more complex, simulating their behaviors becomes computation all complex. But, most modern simulation environments still execute on a single thread, which does not take advantage of the processing power available on modern multi-core CPUs. This paper investigates methods to partition and simulate differential equation-based models of cyber-physical systems using multiple threads on multi-core CPUs that can share data across threads. We describe model partitioning methods using fixed step and variable step numerical in-tegration methods that consider the multi-layer cache structure of these CPUs to avoid simulation performance degradation due to cache conflicts. We study the effectiveness of each parallel simu-lation algorithm by calculating the relative speedup compared to a serial simulation applied to a series of large electric circuit models. We also develop a series of guidelines for maximizing performance when developing parallel simulation software intended for use on multi-core CPUs.
Stochasticity and the Molecular Mechanisms of Induced Pluripotency
Ben D. MacArthur, Colin P. Please, Richard O. C. Oreffo
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003086
Abstract: The generation of induced pluripotent stem cells from adult somatic cells by ectopic expression of key transcription factors holds significant medical promise. However, current techniques for inducing pluripotency rely on viral infection and are therefore not, at present, viable within a clinical setting. Thus, there is now a need to better understand the molecular basis of stem cell pluripotency and lineage specification in order to investigate alternative methods to induce pluripotency for clinical application. However, the complexity of the underlying molecular circuitry makes this a conceptually difficult task. In order to address these issues, we considered a computational model of transcriptional control of cell fate specification. The model comprises two mutually interacting sub-circuits: a central pluripotency circuit consisting of interactions between stem-cell specific transcription factors OCT4, SOX2 and NANOG coupled to a differentiation circuit consisting of interactions between lineage-specifying master genes. The molecular switches which arise from feedback loops within these circuits give rise to a well-defined sequence of successive gene restrictions corresponding to a controlled differentiation cascade in response to environmental stimuli. Furthermore, we found that this differentiation cascade is strongly unidirectional: once silenced, core transcription factors cannot easily be reactivated. In the context of induced pluripotency, this indicates that differentiated cells are robustly resistant to reprogramming to a more primitive state. However, our model suggests that under certain circumstances, amplification of low-level fluctuations in transcriptional status (transcriptional “noise”) may be sufficient to trigger reactivation of the core pluripotency switch and reprogramming to a pluripotent state. This interpretation offers an explanation of a number of experimental observations concerning the molecular mechanisms of cellular reprogramming by defined factors and suggests a role for stochasticity in reprogramming of somatic cells to pluripotency.
Abacavir/lamivudine combination in the treatment of HIV: a review
Geetha Sivasubramanian, Emmanuel Frempong-Manso, Rodger D MacArthur
Therapeutics and Clinical Risk Management , 2010, DOI: http://dx.doi.org/10.2147/TCRM.S1657
Abstract: bacavir/lamivudine combination in the treatment of HIV: a review Review (5040) Total Article Views Authors: Geetha Sivasubramanian, Emmanuel Frempong-Manso, Rodger D MacArthur Published Date February 2010 Volume 2010:6 Pages 83 - 94 DOI: http://dx.doi.org/10.2147/TCRM.S1657 Geetha Sivasubramanian1, Emmanuel Frempong-Manso2, Rodger D MacArthur1 1Division of Infectious Diseases, Wayne State University, Detroit, MI, USA; 2University of Pittsburgh Medical Center, Shadyside Hospital, Pittsburgh, OH, USA Abstract: Abacavir has been at the center of research and clinical interest in the last two years. The frequency of the associated abacavir hypersensitivity syndrome has decreased substantially since the introduction of routine testing for the HLA-B*5701 allele; the activity of the drug in HIV-infected persons with HIV RNA values more than 100,000 copies/mL has been questioned; the possible increased risk of myocardial infarction after recent exposure to abacavir has been debated; and the drug has been moved from the “recommended” category to the “alternative” category in several guidelines. Still, the drug remains a useful agent in combination with other drugs, including lamivudine, for the treatment of HIV infection. This review will focus on the pharmacokinetics, activity, side effects, and resistance profile of both abacavir and lamivudine, including a thorough review of all of the recent studies relevant to both drugs.
Abacavir/lamivudine combination in the treatment of HIV: a review
Geetha Sivasubramanian,Emmanuel Frempong-Manso,Rodger D MacArthur
Therapeutics and Clinical Risk Management , 2010,
Abstract: Geetha Sivasubramanian1, Emmanuel Frempong-Manso2, Rodger D MacArthur11Division of Infectious Diseases, Wayne State University, Detroit, MI, USA; 2University of Pittsburgh Medical Center, Shadyside Hospital, Pittsburgh, OH, USAAbstract: Abacavir has been at the center of research and clinical interest in the last two years. The frequency of the associated abacavir hypersensitivity syndrome has decreased substantially since the introduction of routine testing for the HLA-B*5701 allele; the activity of the drug in HIV-infected persons with HIV RNA values more than 100,000 copies/mL has been questioned; the possible increased risk of myocardial infarction after recent exposure to abacavir has been debated; and the drug has been moved from the “recommended” category to the “alternative” category in several guidelines. Still, the drug remains a useful agent in combination with other drugs, including lamivudine, for the treatment of HIV infection. This review will focus on the pharmacokinetics, activity, side effects, and resistance profile of both abacavir and lamivudine, including a thorough review of all of the recent studies relevant to both drugs.Keywords: HIV, abacavir, lamivudine
Virologic, clinical and immunologic responses following failure of first-line antiretroviral therapy in Haiti
Macarthur Charles,Paul D Leger,Patrice Severe,Colette Guiteau
Journal of the International AIDS Society , 2012, DOI: 10.7448/ias.15.2.17375
Abstract: Background: Since HIV-1 RNA (viral load) testing is not routinely available in Haiti, HIV-infected patients receiving antiretroviral therapy (ART) are monitored using the World Health Organization (WHO) clinical and/or immunologic criteria. Data on survival and treatment outcomes for HIV-1 infected patients who meet criteria for ART failure are limited. We conducted a retrospective study to compare survival rates for patients who experienced failure on first-line ART by clinical and/or immunologic criteria and switched to second-line ART vs. those who failed but did not switch. Methods: Patients receiving first-line ART at the GHESKIO Center in Port-au-Prince, Haiti, who met WHO clinical and immunologic criteria for failure were identified. Survival and treatment outcomes were compared in patients who switched their ART regimen and those who did not. Cox regression analysis was used to determine predictors of mortality after failure of first-line ART. Results: Of 3126 patients who initiated ART at the GHESKIO Center between 1 March 2003 and 31 July 2008, 482 (15%) met WHO immunologic and/or clinical criteria for failure. Among those, 195 (41%) switched to second-line ART and 287 (59%) did not. According to Kaplan–Meier survival analysis, the probability of survival to 12 months after failure of first-line ART was 93% for patients who switched to second-line ART after failure and 88% for patients who did not switch. Predictors of mortality after failure of first-line ART were weight in the lowest quartile for sex, CD4 T cell count≤100, adherence<90% at the time of failure and not switching to second-line ART. Conclusions: Patients who failed first-line ART based on clinical and/or immunologic criteria and did not switch to second-line therapy faced a higher mortality than those who switched after failure. To decrease mortality, interventions to identify patients in whom ART may be failing earlier are needed urgently. In addition, there is a major need to optimize second-line antiretroviral regimens for improved potency, lower toxicity and greater convenience for patients.
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