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Search Results: 1 - 10 of 53111 matches for " David Schade "
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Surface Brightness Evolution of Cluster Galaxies
David Schade
Physics , 1996,
Abstract: Surface brightness evolution has been detected in elliptical galaxies (consistent with passive evolution models of old stellar populations) and in disk galaxies (presumably due to enhanced star-formation rates). The rates of evolution in clusters and the field are not measurably different. In addition to this similarity, the high-redshift populations in both environments exhibit a ``blue-excess'' population, increased rates of star formation, and high frequency of peculiar structure. Thus, there are several parallels between evolving cluster and field galaxies and the high-redshift cluster environment will be understood only by comparison with the field population at the same epoch.
Evidence that Low Density Lipoprotein Is the Primary Cause of Atherosclerotic Cardiovascular Disease: A Bradford-Hill Approach  [PDF]
David S. Schade, Deborah Helitzer, Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2017, DOI: 10.4236/wjcd.2017.79025
Abstract: Cardiovascular disease is the leading cause of death in the Westernized world. The costs in productive lives lost to individuals, families, and society?are?staggering. The epidemiology, pathogenesis, and preventativetreatmentare all clearly described. Why then, has this epidemic not been eradicated? One reason is the uncertainty about the primary cause of atherosclerotic cardiovascular disease. Low density lipoprotein (LDL) is a circulating lipid particle that deposits cholesterol into the arterial wallwhichsubsequently evolves into an atherosclerotic plaque and a life-threatening arterial thrombosis. The reason that LDL is not universally accepted as the cause of atherosclerosisis that there are no randomized controlled trials (RCT’s) providing this evidence. For ethical, financial, and scientificreasons, an RCT of sufficient duration to prove or disprove this hypothesismay never be initiated. We propose aunique approach to support the critical role of LDL in the pathogenesis of cardiovascular disease. Employing criteria based on those proposed by Sir Austin Bradford Hill, we describe the large body of scientific evidence supporting LDL as the primary cause of atherosclerosis. Sir Austin Bradford Hill was a British epidemiologist/statistician who lived in the 20th?century. He acknowledged that the cause of a disease could not always be established by a randomized clinical trial. Therefore, he outlined nine criteria (now known as the Bradford-Hill criteria) that should be met if an etiological factor was likely the cause of a disease. The data in this manuscript are organized according to
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.
Are Lipid Panels Altered by a Large Lunch Meal in Type 2 Diabetes?  [PDF]
Elizabeth Duran-Valdez, Absalon D. Gutierrez, David S. Schade
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2013, DOI: 10.4236/ojemd.2013.32015

Introduction: Recently, analyses of large heterogeneous databases have suggested that there are no differences whether “lipid panels” are drawn in the fed or fasted state, even in diabetic individuals. Whether this is true for individual diabetic patients is unknown. Methods: We studied eight type 2 diabetic individuals and measured serial lipid panels to determine the effect of a large lunch meal. A “Big Mac” equivalent meal was fed to each volunteer and blood for lipid assays was obtained at baseline and hourly for five hours following the meal. Results: The meal induced a significant elevation of glucose, insulin, and c-peptide in each volunteer. In addition, the following lipid parameters significantly changed from baseline concentration during the meal: total cholesterol, non-HDL cholesterol, LDL-cholesterol and triglycerides. Furthermore, the timing of the blood draw post meal also was a determinant of the lipid concentration. No significant concentration change occurred in HDL-cholesterol. Conclusions: In type 2 diabetic patients, lipid panels should be drawn in the fasting state unless the only lipid parameter of interest is HDL-cholesterol.

The Application of the LDL Principle  [PDF]
David S. Schade, Brendan Cavanaugh, Barry Ramo, R. Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2016, DOI: 10.4236/wjcd.2016.65012
Abstract: The LDL Principle has recently been invoked to describe the observation that lowering the LDL cholesterol (by whatever means) results in a lowering of atherosclerotic cardiovascular events. The scientific basis of the LDL Principle dates back to the discovery that the LDL receptor is the prime determinant of the circulating LDL-c concentration. Since that time, major advances have been made at both the basic and clinical science level in our understanding of the pathogenesis and reversal of atherosclerosis. The incorporation of atherogenic lipoproteins plus inflammatory mediators into plaque formation permits the targeted intervention into preventing plaque rupture. In addition, genetic studies identifying individuals with unique phenotypes of either abnormally high or low LDL-c concentrations have provided insight into possible therapeutic modalities that have recently provided the physician with the tools necessary to apply the LDL Principle to achieve reversal of atherosclerosis. The epidemic of atherosclerotic cardiovascular disease has resulted in numerous randomized controlled intervention trials in an attempt to identify approaches to reduce ASCD morbidity and mortality. Recently published data indicate that circulating LDL-c levels of 50 mg/dl or less are not only physiologic at birth but also effective in greatly reducing cardiovascular disease. In addition, the recent availability of two PCSK9 inhibitors provides the primary care physician with the possibility of achieving this low level of LDL-c even in statin intolerant patients. The widespread availability of the coronary artery calcium scan plus the inclusion of traditional cardiovascular risk factors in risk assessment has enabled the physician to readily identify asymptomatic individuals at high risk for cardiovascular events. Aggressively applying the LDL Principle to these individuals has the potential of greatly reducing cardiovascular mortality. This review will document the scientific basis for this principle and provide the arguments in favor of its aggressive application.
A Pediatric Opportunity in Adolescents to Prevent Adult Heart Attacks  [PDF]
David S. Schade, Shirley Murphy, Vernat Exil, R. Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2018, DOI: 10.4236/wjcd.2018.82009
Abstract: Importance: Cardiovascular disease is the number one cause of death in the adult population, greater than all cancers combined. When a heart attack or stroke occurs, many individuals have no advance warning, thus making prevention difficult. Cardiovascular disease begins early, i.e., in the developing fetus, and progresses throughout childhood and adolescence, such that it is identifiable both radiographically and ultrasonographically in the adolescent. Observations: There are multiple lines of evidence that atherosclerosis is present in the pediatric population. This evidence is based on autopsy studies in accident victims, coronary artery calcium scoring and carotid intermedia thickness measurements, intravascular ultrasound studies of hearts transplanted from teenage accident victims, and wartime casualties in young males. Multiple studies of cardiovascular risk factors (e.g., hypertension, obesity, insulin resistance, glucose intolerance and hyperlipidemia) have emphasized their importance in contributing to the pathogenesis of atherosclerosis. With the recent increase of obesity in the pediatric population, these risk factors will assume increasing importance in the development of clinical cardiovascular disease in the adult population. Prevention of atherosclerosis will require measuring a lipid profile in adolescents and initiating intervention to reduce the triglyceride and LDLc concentration. Education of both the adolescent at risk and his/her family will be necessary. Lifestyle changes are paramount. Hyperlipidemic medication should be reserved for individuals with severe lipid abnormalities. Conclusion and Relevance:Atherosclerotic changes of arteries begin during gestation and progress throughout the pediatric years into adulthood. Pediatricians’ contribution to reducing the progression of atherosclerosis in their
In Defense of the LDL Hypothesis  [PDF]
David S. Schade, Lynda Shey, R. Philip Eaton
World Journal of Cardiovascular Diseases (WJCD) , 2019, DOI: 10.4236/wjcd.2019.93022
Abstract: Both clinical and basic science studies during the last 30 years have emphasized the importance of cholesterol in the pathogenesis of atherosclerosis. There is a direct relationship between the level of circulating cholesterol (as LDLc remnant particles) and the incidence of cardiovascular events. However, this hypothesis has not gone unchallenged, both in social media and the scientific literature. This controversy has major consequences to the health of the public,?because atherosclerosis is the number one cause of morbidity and mortality in the Western World.?The proponents of the non-importance of atherosclerosis base their argument on certain studies. We have carefully examined these studies in order to address the validity of the challenges.?Each of these studies has its own deficiencies?as pointed out in this article. Overall, the evidence that cholesterol is not the primary underlying pathogenic factor causing heart attacks and strokes is based on a flawed interpretation of study results. These studies have several serious deficiencies including lost data, inadequate power, excessive drop outs, borderline significance, and lack of a control group. The conclusion that cholesterol is essential in the pathogenesis of atherosclerosis is critical for treating and preventing atherosclerosis and reducing the prevalence of cardiovascular disease.
Discovery of a New Quadruple Lens HST 1411+5211
Philippe Fischer,David Schade,Felipe Barientos
Physics , 1998, DOI: 10.1086/311555
Abstract: Gravitational lensing is an important tool for probing the mass distribution of galaxies. In this letter we report the discovery of a new quadruple lens HST 1411+5211 found in archived WFPC2 images of the galaxy cluster CL140933+5226. If the galaxy is a cluster member then its redshift is $z=0.46$. The images of the source appear unresolved in the WFC implying that the source is a quasar. We have modeled the lens as both a single galaxy and a galaxy plus a cluster. The latter model yields excellent fits to the image positions along with reasonable parameters for the galaxy and cluster making HST 1411+5211 a likely gravitational lens. Determination of the source redshift and confirmation of the lens redshift would allow us to put strong constraints on the mass distribution of the lensing galaxy.
Internal Kinematics of Blue CFRS Galaxies at z ~ 0.6
Gabriela Mallen-Ornelas,Simon Lilly,David Crampton,David Schade
Physics , 1999,
Abstract: We present the results of a study of the internal kinematics of luminous starforming galaxies in the 0 < z < 0.8 range, with the aim of investigating the nature of the blue galaxies which cause the largest changes in the luminosity function at z > 0.5. New kinematic data are analysed for a sample of 24 galaxies from the Canada-France Redshift Survey, most of them with rest-frame (U-V)_{AB}< 1.14. Unlike most previous studies, target galaxies were selected regardless of size and morphology, from a well-studied magnitude-limited survey (the CFRS). Our sample is therefore representative of the most rapidly changing 1/3 of the galaxy population in the 0 < z < 0.8 range. The 15 galaxies at z > 0.45 have sizes (from HST images) and velocity widths sigma_{v} (from emission lines) similar to those of typical local Irregulars. This is consistent with their morphologies and rest-frame colors; however, these galaxies are as bright as the brightest local Irregulars, and roughly 2 magnitudes brighter than typical Irregulars known nearby. We conclude that the increase in the number density of luminous blue galaxies at z > 0.5 is mainly due to a population of small and unusually-bright late-type galaxies.
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