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Search Results: 1 - 10 of 298244 matches for " J. Elliott "
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Flaws, Fallacies and Facts: Reviewing the Early History of the Lipid and Diet/Heart Hypotheses  [PDF]
J. Elliott
Food and Nutrition Sciences (FNS) , 2014, DOI: 10.4236/fns.2014.519201
Abstract: The lipid hypothesis of coronary heart disease proposes that a high total cholesterol level has a causative role in coronary heart disease (CHD), specifically in the development of atherosclerosis. It forms the basis for formulating target levels of serum cholesterol and hence the widespread use of statins for lowering cholesterol. An extension of the lipid hypothesis is the diet/heart hypothesis of coronary heart disease. This theory combines two ideas—that saturated fat raises cholesterol levels, and that a reduced saturated fat intake will lower cholesterol levels, thereby inhibiting the development of atherosclerosis and manifestations of CHD. Those who make diet recommendations or prescribe medication to reduce cholesterol may be unaware of the underpinning science. The original research behind these recommendations has given us “healthy heart” guidelines and preventive measures we assume to be true. While the lipid and diet/heart hypotheses are often presented as fact, they remain inadequately proven theories that have little agreement from experts. Historical perspectives can help us understand the basis of current-day beliefs. In the lipid hypothesis case, research from the 1950s and 60s was instrumental in its formation. This early work should not be considered irrelevant, outdated or obsolete because current recommendations from national heart associations in many countries continue to be shaped by these studies. This paper examines evidence used to formulate the lipid hypothesis and, subsequently, the diet/ heart hypothesis. By critically evaluating steps in the formation of the theory, inconsistencies, mistakes and alternate explanations become apparent and cast doubt on its validity.
The Sociological Determination: A Reflexive Look at Conducting Local Disaster Research after Hurricane Katrina  [PDF]
Timothy J. Haney, James R. Elliott
Sociology Mind (SM) , 2013, DOI: 10.4236/sm.2013.31002

This paper examines the process of collecting data on New Orleanians affected by Hurricane Katrina. It does so by focusing upon the experiences of local researchers who were simultaneously conducting research on and within the disaster. It also documents one research team’s attempt to generate a random sample of residents from several New Orleans neighborhoods, stratified both by racial composition and level of damage. Further, it describes the challenges associated with navigating complex bureaucracies that are themselves affected by the disaster. Results demonstrate that our methods for drawing samples from six New Orleans neighborhoods yielded highly representative samples, even in heavily damaged neighborhoods where the long-term displacement required a multi-pronged strategy that involved contact by mail, telephone, and visits to local churches. The paper concludes by making recommendations for facilitating future research by locally affected researchers.


Thermodynamics of the Reduction Roasting of Nickeliferous Laterite Ores  [PDF]
R. Elliott, C. A. Pickles, J. Forster
Journal of Minerals and Materials Characterization and Engineering (JMMCE) , 2016, DOI: 10.4236/jmmce.2016.46028
Abstract: The global nickel sulphide resources are becoming more difficult to mine and, as a result, there is increasing interest in the current and future development of the oxidic nickel laterite deposits. In comparison to the sulphide ores, the nickel laterites cannot be readily upgraded by conventional means and growing attention is being focused on the development of new methods for processing these ores. In this paper, firstly, brief overviews of laterite ore mineralogy and the conventional techniques used to extract the nickel from both the limonitic and the saprolitic nickeliferous laterites are provided. Secondly, previous research on the thermodynamic modelling of the reduction of the laterites is discussed. Thirdly, an improved thermodynamic model is used to predict the equilibrium products arising from the solid state reduction of both the limonitic and the saprolitic ores. Based on these thermodynamic predictions, the reduction behaviors of the two ore types are compared in terms of nickel recovery and grade in the ferronickel product. The effects of reduction temperature, ore composition and carbon additions were studied. Finally, the results from the simulations are compared to the experimental data available in the literature.
The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development
J Elliott Scott
Tobacco Induced Diseases , 2004, DOI: 10.1186/1617-9625-2-1-3
Abstract: Tobacco in various forms, as well as tobacco-related compounds such as marijuana, represent agents that present serious and insidious health risks to the general population. Both of these drugs have long and interesting histories. As this review is focused primarily on tobacco, marijuana use will be discussed only as it reflects on health effects resulting from both tobacco and marijuana. Tobacco use passed into Europe in the late sixteenth century after initial encounters between Europeans and native North and South Americans [1]. Tobacco was seen often as a medicine. Several well known European physicians extolled the virtues of tobacco as a medicinal herb [1] and tobacco enemas were recommended for treatment of cholera and to loosen the bowels [2]. Ironically, one of among some twenty ailments purportedly amenable to tobacco was cancer [2]. For the next two centuries modest changes in cultivation, largely in the American colonies, provided increasing supplies of tobacco to Europe although it should be noted that consumption was taken largely in the form of chewing plugs [2], snuffed, or smoked in pipes [3]. It was not until the late 1860's that a sudden change in consumption occurred. In fact the change was startling. According to Tilley [4], in 1869 about 2 million cigarettes were being manufactured in the United States and it was uncommon to see someone smoking in public. Some ten years later with the advent of new curing methodologies, the introduction of the Bonsack cigarette-making machine, and as the cigarette fashion took hold, 300 million units were produced. Indeed, the Bonsak machine could produce some 100,000 cigarettes a day, the equivalent of the work of 30–40 labourers. These machines marked an innovative turning point for the tobacco industry [5]. The production level initiated by the automated machines was reflected in the consumption trend as tobacco sales between the late nineteenth century until the end of the first World War underwent a major
Tobacco Induced Diseases moves to BioMed Central
J Elliott Scott
Tobacco Induced Diseases , 2008, DOI: 10.1186/1617-9625-4-1
Abstract: Alongside this article, the first articles accepted by Tobacco Induced Diseases are published on BioMed Central's open access publishing platform. Until now, the journal has been hosted at the University of Manitoba in Winnipeg, Canada. The journal and its host society, the International Society for the Prevention of Tobacco Induced Diseases (ISPTID), have an interesting history [1]. Originally founded as a forum for exchange of information concerning a common interest in the prevention of disease induced by cigarette smoking, this society has transformed into an internationally recognized group of experts on international anti-smoking law implementation and enforcement efforts. In addition, we are now mounting an effort to extend our publication efforts into the areas of basic biological effects of tobacco smoke constituents. As a scientist who primarily undertakes research in this latter category, I find myself at the society meetings in a somewhat foreign environment. In the presence of policy and epidemiological experts and analysts, a basic biomedical scientist hears about duplicitous dealings of tobacco companies, shifts in cigarette use demographics, and, most importantly, real impacts, including fatal impacts, of smoking on populations and individuals. For a molecular researcher this is indeed new territory and has become an interesting experience, a foray out of the laboratory and maybe a chance to find the much sought-after relevance for all the work of students, technicians and collaborators. Indeed, the ISPTID has provided a growing international platform to explore many aspects of disease induced by tobacco smoke. For this reason, as well as to stress the emphasis on molecular research in the medical literature, we have expanded our editorial research board to include Xing Li Wang who brings scientific credibility in the area of vascular genetics, cell and molecular biology. Dr. Wang is Professor of Surgery in the Cardiothoracic Surgery Division of the
Scott J Elliott
Tobacco Induced Diseases , 2005, DOI: 10.1186/1617-9625-3-1
The "New Journal" dilemma
Scott J Elliott
Tobacco Induced Diseases , 2006, DOI: 10.1186/1617-9625-3-55
The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development
Scott J Elliott
Tobacco Induced Diseases , 2004, DOI: 10.1186/1617-9625-2-1
Abstract: Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactant are the first body tissues to be directly exposed to the many thousands of toxic chemicals in tobacco. Considering the vast surface area of the lung and the extreme attenuation of the blood-air barrier, it is not surprising that this organ is the primary route for exposure, not just to smoke but to most environmental contaminants. Recent research has shown that the pulmonary surfactant, a complex mixture of phospholipids and proteins, is the first site of defense against particulates or gas components of smoke. However, it is not clear what effect smoke has on the surfactant. Most studies have demonstrated that smoking reduces bronchoalveolar lavage phospholipid levels. Some components of smoke also appear to have a direct detergent-like effect on the surfactant while others appear to alter cycling or secretion. Ultimately these effects are reflected in changes in the dynamics of the surfactant system and, clinically in changes in lung mechanics. Similarly, exposure of the developing fetal lung through maternal smoking results in postnatal alterations in lung mechanics and higher incidents of wheezing and coughing. Direct exposure of developing lung to nicotine induces changes suggestive of fetal stress. Furthermore, identification of nicotinic receptors in fetal lung airways and corresponding increases in airway connective tissue support a possible involvement of nicotine in postnatal asthma development. Finally, at the level of the alveoli of the lung, colocalization of nicotinic receptors and surfactant-specific protein in alveolar cells is suggestive of a role in surfactant metabolism. Further research is needed to determine the mechanistic effects of smoke and its components on surfactant function and, importantly, the effects of smoke components on the developing pulmonary system.
The "New Journal" dilemma
Scott J Elliott
Tobacco Induced Diseases , 2006, DOI: 10.1186/1617-9625-3-2-1
Marathon pacing and elevation change
J. B. Elliott
Physics , 2012,
Abstract: An analysis of marathon pacing and elevation change is presented. It is based on an empirical observation of how the pace of elite and non-elite marathon runners change over the course of the marathon and a simple approximation of the energy cost of ascent and decent. It was observed that the pace of the runners slowed in a regular manner that could be broken up into four regions. That observation can be used to project target paces for a desired marathon finish time. However, that estimate fails to take in to account the energetic costs of elevation changes (hills) along the marathon course. Several approximations are made to give a coarse estimate of target paces for marathon run on courses with significant elevation changes, i.e. a hilly course. The 2012 Oakland Marathon course is used as and example of a hilly course and the times of 23 finishers are examined.
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