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Search Results: 1 - 10 of 270027 matches for " David R. Kamerschen "
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Unemployment Benefits and Unemployment  [PDF]
William Beranek, David R. Kamerschen
Modern Economy (ME) , 2011, DOI: 10.4236/me.2011.25088
Abstract: This paper seeks to provide a simpler explanation of the Match Quality Hypothesis (MQH). For the less mathematically inclined, it avoids formal analysis and yet derives the relevant implications, i.e., if unemployed workers currently collecting unemployment benefits are given more benefits, both the average period of unemployment duration increases as well as the level of unemployment. To produce these effects, only one person behaving in this manner is required. We cite recent evidence supporting these implications. Examined are implications of this theorem for both U.S. and European regions where, in some cases, voluntarily unemployed workers are eligible for unemployment benefits. We question the importance of the notion that generous unemployment benefits that intensify searches for better jobs, and hence prolonged job searches, ultimately yield societal benefits.
Development of the Higher Education Value Inventory: Factor Structure and Score Reliability  [PDF]
Vickie R. Luttrell, David C. S. Richard
Psychology (PSYCH) , 2011, DOI: 10.4236/psych.2011.29137
Abstract: Students bring to college a value system that affects their levels of academic achievement and persistence. The goal of this project was to develop a self-report inventory that measures the value students place on higher education. The Higher Education Value Inventory (HEVI) surveys students’ attitudes and behaviors in five domains: family expectations, scholastic focus, achievement value, general education value, and achievement obstacles. We describe the development of the HEVI and report the results of reliability studies and factor analyses. HEVI scores accounted for 35.9% of the variance in freshman grades. Implications for educational researchers and admissions officers are provided
Testing for a Zero Proportion  [PDF]
Jonathan R. Bradley, David L. Farnsworth
Open Journal of Statistics (OJS) , 2013, DOI: 10.4236/ojs.2013.34029
Abstract: Tests for a proportion that may be zero are described. The setting is an environment in which there can be misclassifications or misdiagnoses, giving the possibility of nonzero counts from false positives even though no real examples may exist. Both frequentist and Bayesian tests and analyses are presented, and examples are given.
Gentamicin Renal Excretion in Rats: Probing Strategies to Mitigate Drug-Induced Nephrotoxicity  [PDF]
Aruna Dontabhaktuni, David R. Taft, Mayankbhai Patel
Pharmacology & Pharmacy (PP) , 2016, DOI: 10.4236/pp.2016.71007
Abstract: The renal excretion of gentamicin, an aminoglycoside antibiotic, was studied in the isolated perfused rat kidney (IPRK) model. Dose-linearity experiments were carried out at four doses (400, 800, 1600, 3200 μg), targeting initial perfusate levels of 5, 10, 20 and 40 μg/ml. Additionally, gentamicin was co-perfused with sodium bicarbonate (0.25 mM) and/or cimetidine (2 mM) to evaluate the effect of urinary alkalization and secretory inhibition on gentamicin excretion and kidney accumulation. Gentamicin displayed net reabsorption in the IPRK, consistent with extensive luminal uptake. Kinetic analysis indicated that luminal transport of gentamicin (kidney ? urine) is the rate-determining step for gentamicin urinary excretion. Clearance and cumulative excretion decreased with increased gentamicin dose. Gentamicin kidney accumulation, estimated by mass balance, ranged from ~20% - 30%. Urinary alkalization significantly increased gentamicin excretion, with no effect on kidney accumulation. Conversely, cimetidine co-administration did not affect gentamicin clearance in the IPRK, but kidney accumulation was significantly reduced. When both sodium bicarbonate and cimetidine were administered together, gentamicin kidney accumulation decreased ~80% with corresponding increases in clearance and excretion ratio (XR) compared to gentamicin alone. A main strategy to reduce the incidence of nephrotoxicity with gentamicin therapy (up to ~25%) involves reducing kidney accumulation of the compound. The results of this research suggest that the combination of urinary alkalization and inhibition of basolateral secretion (blood → kidney) may be a viable approach to mitigate aminoglycoside toxicity, and warrants further investigation.
Residual Cardiovascular Risk—Is Inflammation the Primary Cause?  [PDF]
David S. Schade, R. Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2018, DOI: 10.4236/wjcd.2018.81007
Abstract: Every cardiovascular clinical trial that has examined the beneficial effects of lowering LDL cholesterol to prevent cardiovascular events has demonstrated residual cardiovascular risk in the interventional treatment group. Residual risk is the term applied to the cardiovascular events (e.g., myocardial infarction, stroke, and cardiovascular death) that occur in spite of being on “optimal” medical therapy. This term is usually applied to secondary intervention studies,?i.e., lipid lowering treatments in subjects who have already had at least one cardiovascular event. Studies that described residual risk have attributed it, at least in part, to the fact that the LDLc has not been lowered sufficiently to stop atherosclerotic plaque formation and rupture into the arterial lumen. However, a recent cardiovascular intervention clinical trial which achieved a very low group median LDLc of 30 mg/dl still demonstrated significant residual risk. Of more importance to reducing residual risk may be addressing the ongoing inflammation in the coronary arteries that results in cellular liberation of cytokines and proteases that attack the atherosclerotic plaque’s fibrous cap. Recent studies have shown that inflammation may act independently of LDL to cause cardiovascular events. This article provides evidence that inflammation is the primary cause of residual risk and will need to be treated as aggressively as LDL lowering if CVD events in the post treatment period are to be significantly reduced. Addressing major risk factors including obesity, diabetes, smoking, hypertension and hyperlipidemia are critical to reducing inflammation. Statins and aspirin are the mainstay medications to reduce ongoing inflammation. However, newer pharmaceuticals may also be required to reduce inflammation to undetectable levels. Targeting inflammation to eradicate residual cardiovascular risk will be the next therapeutic challenge facing primary care physicians.
The Basis of Atherosclerotic Guidelines—Time for a Change?  [PDF]
David S. Schade, R. Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2018, DOI: 10.4236/wjcd.2018.87033
Abstract: Major advances have occurred within the last decade in the understanding of the pathogenesis of coronary artery disease. Not only are the underlying mechanisms now clearly defined, but effective medical therapies are available at low cost and minimal side effects. In spite of these advances, cardiovascular events are still the leading cause of death in the United States and the Western world. Analysis of the many factors involved in the delivery of appropriate cardiovascular care strongly suggests that the primary reason is the overly restrictive guidelines published by medical societies. This article proposes a much broader basis for constructing atherosclerosis clinical guidelines, namely the known pathophysiology of atherosclerosis. If pathophysiology forms the basis of atherosclerotic treatment recommendations, then a risk/benefit analysis can be used to determine appropriate preventive therapy for any specific individual. The result will be that many additional individuals will be eligible for preventive treatment of atherosclerosis, and the saving of many lives at minimal cost will result.
On Multiplicative Sidon Sets
David Wakeham,David R. Wood
Mathematics , 2011,
Abstract: Fix integers $b>a\geq1$ with $g:=\gcd(a,b)$. A set $S\subseteq\mathbb{N}$ is \emph{$\{a,b\}$-multiplicative} if $ax\neq by$ for all $x,y\in S$. For all $n$, we determine an $\{a,b\}$-multiplicative set with maximum cardinality in $[n]$, and conclude that the maximum density of an $\{a,b\}$-multiplicative set is $\frac{b}{b+g}$. For $A, B \subseteq \mathbb{N}$, a set $S\subseteq\mathbb{N}$ is \emph{$\{A,B\}$-multiplicative} if $ax=by$ implies $a = b$ and $x = y$ for all $a\in A$ and $b\in B$, and $x,y\in S$. For $1 < a < b < c$ and $a, b, c$ coprime, we give an O(1) time algorithm to approximate the maximum density of an $\{\{a\},\{b,c\}\}$-multiplicative set to arbitrary given precision.
Multisized Inert Particle Loading for Solid Rocket Axial Combustion Instability Suppression
David R. Greatrix
International Journal of Aerospace Engineering , 2012, DOI: 10.1155/2012/173129
Abstract: In the present investigation, various factors and trends, related to the usage of two or more sets of inert particles comprised of the same material (nominally aluminum) but at different diameters for the suppression of axial shock wave development, are numerically predicted for a composite-propellant cylindrical-grain solid rocket motor. The limit pressure wave magnitudes at a later reference time in a given pulsed firing simulation run are collected for a series of runs at different particle sizes and loading distributions and mapped onto corresponding attenuation trend charts. The inert particles’ presence in the central core flow is demonstrated to be an effective means of instability symptom suppression, in correlating with past experimental successes in the usage of particles. However, the predicted results of this study suggest that one needs to be careful when selecting more than one size of particle for a given motor application. 1. Introduction Over the last number of decades, a multitude of research efforts have been directed towards understanding the physical mechanisms, or at least the surrounding factors, behind the appearance of symptoms typically associated with nonlinear axial combustion instability in solid-propellant rocket motors (SRMs). The principal symptoms are the presence within the motor chamber of stronger finite-amplitude traveling axial pressure waves that may be shock fronted, commonly (although not always) accompanied by some degree of base chamber pressure rise (dc shift). Note that low-magnitude pressure waves due to vortex shedding from segmented/gapped components in the motor chamber are not included (here) in this more traditional category of nonlinear axial instability. Studies of nonlinear axial combustion instability have ranged from numerous experimental test firing series on the one hand [1–3], and linear/nonlinear acoustic theory modeling on the other (largely, the analysis producing frequency-based standing wave solutions for a given chamber geometry, but without some useful quantitative information) [4–7]. On occasion, researchers have employed a numerical modeling approach, to work towards a more comprehensive quantitative understanding of the physics involved (the numerical model producing a traveling wave solution to a limit wave amplitude and corresponding small or larger dc shift, typically a time-based result evolving from an initial pulse disturbance introduced into the chamber flow) [8, 9]. Available computational power and associated result turnaround times commonly forced some simplifications in the
Transient Burning Rate Model for Solid Rocket Motor Internal Ballistic Simulations
David R. Greatrix
International Journal of Aerospace Engineering , 2008, DOI: 10.1155/2008/826070
Abstract: A general numerical model based on the Zeldovich-Novozhilov solid-phase energy conservation result for unsteady solid-propellant burning is presented in this paper. Unlike past models, the integrated temperature distribution in the solid phase is utilized directly for estimating instantaneous burning rate (rather than the thermal gradient at the burning surface). The burning model is general in the sense that the model may be incorporated for various propellant burning-rate mechanisms. Given the availability of pressure-related experimental data in the open literature, varying static pressure is the principal mechanism of interest in this study. The example predicted results presented in this paper are to a substantial extent consistent with the corresponding experimental firing response data.
HIV Neurotoxicity: Potential Therapeutic Interventions
David R. Wallace
Journal of Biomedicine and Biotechnology , 2006, DOI: 10.1155/jbb/2006/65741
Abstract: Individuals suffering from human immunodeficiency virus type 1 (HIV-1) infection suffer from a wide range of neurological deficits. The most pronounced are the motor and cognitive deficits observed in many patients in the latter stages of HIV infection. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. One of the more debilitating of the HIV-related syndromes is AIDS-related dementia, or HAD. Complete understanding of HIV neurotoxicity has been elusive. Both direct and indirect toxic mechanisms have been implicated in the neurotoxicity of the HIV proteins, Tat and gp120. The glutamatergic system, nitric oxide, calcium, oxidative stress, apoptosis, and microglia have all been implicated in the pathogenesis of HIV-related neuronal degeneration. The aim of this review is to summarize the most recent work and provide an overview to the current theories of HIV-related neurotoxicity and potential avenues of therapeutic interventions to prevent the neuronal loss and motor/cognitive deficits previously described.
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