Hamlet and Archilles - 1101 Words

The truly great human stories deal with the most basic elements of human emotions and motivations. The Following stories are perfect examples of those elements. Revenge, love, lust, betrayal, loss and grief are all powerful storytelling tools and powerful elements within stories. But stories are also specific, about specific people, specific times and specific cultures. The Iliad is a sweeping war story that ends in the victory of the Greeks even at great costs for the victors. Hamlet is more of a personal tragedy that ends in defeat and death for all. The major players might seem like they could not be more distinct upon their face. But, in fact, the characters of Achilles and Hamlet have notable similarities. They are both ultimately spurred to their pivotal decisions and behaviors by the feeling of vengeance, connected to a strong feeling of duty and even a sense of piety. Yet, because Achilles is a soldier and Hamlet an intellectual prince, their ultimate motivations and actions vary wildly in terms of timing, execution, approach and ultimate success, even though both men are ultimately killed as a result of their actions. Hamlet and Achilles each respond to the death of a person close to them. Hamlet has lost his father, and we see in the beginning of the play that he suffers from a deep melancholy, which Hazen 2

What Is It s One Of The Big Question About Human Existence

What is Meaningful? Philosophy-1301-001 Charles Clinton Hinkley 5/31/2015 The meaning of life. It’s one of the big questions in philosophy, one of the big questions about human existence. A big part of the Christians or at least to (Page,2015) Page is to believes â€Å"the meaning of life is to fulfill God’s will, live our lives, have a career, make a family, have fun, and then die at the time God appointed for us to die.† (Page, Pg. 1) To some atheist, their belief is that there’s no meaning to life. They believe in evolution, to survive and reproduce. That we’re just a tiny spec of this huge universe. â€Å"It is more important to find what makes this life precious and worth living, rather than hoping that the â€Å"next one† will be better.†(AFA).†¦show more content†¦Since everything in creation came from this God, it too would automatically have meaning and purpose. God’s own individual purpose or meaning is unknown to us, except some people believe that God creates us, loves us, and wants to fellowship with us in eternity. He is the only supreme God, and He has always existed. In the beginning, God is the only thing that existed. If God has meaning, we can assume the environment around us have meaning. If God has a plan, then we can assume everything else that has come into existence has a purpose in that plan. God is sovereign. The meaning of life is similar to a person building something. If a person collects wood, buy tools, and then proceed to hammer the wood together, we can assume that the creation is going to be there for a reason. He or she may be building a house, or a storage building, etc. But none of us would suggest that the man is building it for nothing. Any reasonable person would logically conclude that the man has a purpose for his creation. It was created with purpose in mind. Going back to the introduction, Atheist say that there isn’t a meaning to life. You’re just a tiny grain of sand compared to the universe that we live in. Relaying on evolution to be able to keep surviving and reproducing, to continue to live. If God does not exist,

Surface Pressure Measurements on an Aerofoil Free Essays

DEN 302 Applied Aerodynamics SURFACE PRESSURE MEASUREMENTS ON AN AEROFOIL IN TRANSONIC FLOW Abstract The objective of this exercise is to measure the pressure distribution across the surface on an aerofoil in a wind tunnel. The aerofoil is tested under several different Mach numbers from subsonic to supercritical. The purpose of measuring the pressure distributions is to assess the validity of the Prandtl-Glauert law and to discuss the changing chracteristics of the flow as the Mach number increases from subsonic to transonic. We will write a custom essay sample on Surface Pressure Measurements on an Aerofoil or any similar topic only for you Order Now As a result of the experiment and computation of data, the aerofoil was found to have a critical Mach number of M=0. 732. Below this freestream Mach number the Prandtl-Glauert law predicted results very successfully. However, above this value, the law completely breaks down. This was found to be the result of local regions of supersonic flow and local shockwaves. Contents Abstract2 Apparatus2 1. Induction Wind Tunnel with Transonic Test Section2 2. Aerofoil model3 3. Mercury manometer3 Procedure3 Theory3 Results4 Discussion8 Transonic Flow8 Analysis9 Conclusion11 Bibliography11 Apparatus 1. Induction Wind Tunnel with Transonic Test Section The tunnel used in this experiment has a transonic test section with liners, which, after the contraction, remain nominally parallel bar a slight divergence to accommodate for boundary layer growth on the walls of the test section. The liners on the top and bottom are ventilated with longitudinal slots backed by plenum chambers to reduce interference and blockage as the Mach number increase to transonic speeds. The working section dimensions are 89mm(width)*178mm(height). The stagnation pressure , p0? is close to the atmospheric pressure of the lab and with only a small error ,is taken to be equal to the settling chamber pressure. The reference staticpressure, p? , is measured via a pressure tapping in the floor of the working section, well upstream of the model so as to reduce the disturbance due to the model. The ‘freestream’ Mach number, M? , can be calculated by the ratio of static to stagnation pressure. The tunnel airspeed is controlled by varying the pressure of the injected air, with the highest Mach number that can be achieved by the tunnel being 0. 88. 2. Aerofoil model The model used is untapered and unswept, having the NACA 0012 symmetric section. The model chord length, c, is 90mm and the model has a maximum chord/thickness ratio of 12%. Non-dimensionalised co-ordinates of the aerofoil model are given in table 1 below. Pressure tappings, 1-8 , are placed along the upper surface of the model at the positions detailed in table 1. An additional tapping, 3a, is placed on the lower surface of the aerofoil at the same chordwise position as tapping 3. The reason for including the tapping on the lower surface is so that the model can be set at zero incidence by equalizing the pressures at 3 and 3a 3. Mercury manometer A multitube mercury manometer is used to record the measurements from the tappings on the surface of the model. The manometer has a ‘locking’ mechanism which allows the mercury levels to be ‘frozen’ so that readings can be taken after the flow has stopped. This is useful as the wind tunnel is noisy. The slope of the manometer is 45 degrees. Procedure The atmospheric pressure is first recorded, pat, in inches of mercury. For a range of injected pressures, Pj, from 20 to 120Psi, the manometer readings are recorded for stagnation pressure (I0? , reference static pressure (I? ), and surface pressure form tappings on the model (In, for n=1-8 and 3a). Theory These equations are used in order to interpret and discuss the raw results achieved from the experiment. To convert a reading, I, from the mercury manometer into an absolute pressure, p, the following is used: p=pat ±l-latsin? (1) For isentropic flow of a perfect gas with ? =1. 4, the frees tream Mach number,M? , is related to the ratio between the static and stagnation pressures by the equation: M? =2? -1p? p0? -? -1? -1. 0(2) Pressure coefficient, Cp , is given by: Cp=p-p? 12 U? 2(3) For compressible flow this can be rewritten as: Cp=2? M? 2pp? -1(4) The Prandtl-Glauert law states that the pressure coefficient, CPe, at a point on an aerofoil in compressible, sub-critical flow is related to the pressure coefficient, CPi, at the same point in in incompressible flow by the equation: CPe=CPi1-M? 2(5) Due to its basis in on thin aerofoil theory, this equation does not provide an exact solution. However it is deemed reasonably accurate for cases such as this in which thin aerofoils are tested at small incidence. The law does not hold in super-critical flow when local regions of supersonic flow and shockwaves appear. The value of the critical pressure coefficient, Cp*, according to local sonic conditions is calculated by: Cp*=10. 7M? 25+M? 263. 5-1for? =7/5(6) The co-ordinates for the NACA 0012 section are as follows: Figure 1-Co-ordinates for aerofoil (Motallebi, 2012) Results Given atmospheric conditions of: Patm=30. 65 in-Hg Tatm=21 °C The following results were achieved: Figure 2-Pressure coefficient vs x/c for M=0. 83566 Figure 3-Pressure coefficient vs x/c for M=0. 3119 Figure 4-Pressure coefficient vs x/c for M=0. 79367 Figure 5-Pressure coefficient vs x/c for M=0. 71798 Figure 6-Pressure coefficient vs x/c for M=0. 59547 Figure 7-Pressure coefficient vs x/c for M=0. 44456 Figure 8-Cp* and Cpminvs Mach Number From figure 7 the critical Mach number is able to be determined. The critical Mach number (the maximum velocity than can be achieved before local shock conditions arise) occurs at the point where the curves for Cp* and Cpmin cross. From figure 7 we can see that this value is, M? =0. 732. Discussion Transonic Flow Transonic flow occurs when ‘there is mixed sub and supersonic local flow in the same flow field. ’ (Mason, 2006) This generally occurs when free-stream Mach number is in the range of M=0. 7-1. 2. The local region of supersonic flow is generally ‘terminated’ by a normal shockwave resulting in the flow slowing down to subsonic speeds. Figure 8 below shows the typical progression of shockwaves as Mach number increases. At some critical Mach number (0. 72 in the case of Figure 8), the flow becomes sonic at a single point on the upper surface of the aerofoil. This point is where the flow reaches its highest local velocity. As seen in the figure, increasing the Mach number further, results in the development of an area of supersonic flow. Increasing the Mach number further again then moves the shockwave toward the trailing edge of the aerofoil and a normal shockwave will develop on the lower surface of the aerofoil. As seen in figure 8, approaching very close to Mach 1, the shockwaves move to the trailing edge of the aerofoil. For M1, the flow behaves as expected for supersonic flow with a shockwave forming at the leading edge of the aerofoil. Figure 9-Progression of shockwaves with increasing Mach number (H. H. Hurt, 1965) In normal subsonic flow, the drag is composed of 3 components-skin friction drag, pressure drag and induced drag. The drag in transonic is markedly increased due to changes to the pressure distribution. This increased drag encountered at transonic Mach numbers is known as wave drag. The wave drag is attributed to the formation of local shockwaves and the general instability of the flow. This drag increases at what is known as the drag divergence number (Mason, 2006). Once the transonic range is passed and true supersonic flow is achieved the drag decreases. Analysis From figure 7, the conclusion was reached that the critical Mach number was 0. 732. This means ultimately that in the experiment local shockwaves should be experienced somewhere along the aerofoil for Mach numbers M=0. 83566, 0. 83119 and 0. 79367. According to transonic theory, these shockwaves should be moving further along the length of the aerofoil as the freestream Mach number increases. To determine the approximate position of the shockwaves it is useful to look again at equation (4). Cp=2? M? 2pp? -1 Assuming constant p? , as static pressure in the test section is assumed to be constant and constant free stream Mach number as well, equation (4) may be written as: Cp=const. pconst. -1 Normal shockwaves usually present themselves as discontinuous data, particularly in stagnation pressure where there is a large drop. To detect the rough position of the shockwave on the aerofoil surface it is useful to look at the detected pressure by the different tappings and scrutinize the –Cpvs x/c graph to see where the drop in pressure occurs. Investigating the graphs for the supercritical Mach numbers yields these approximate positions: M| x/c, %| 0. 835661| 40-60| 0. 831199| 35-55| 0. 793676| 25-45| Figure 10- Table showing approximate position of shockwave According to the theory described earlier, these results are correct as it demonstrates the shockwave moving further along the aerofoil as the Mach number increases. As seen in figure 8, given a sufficiently high Mach number, a shock may also occur on the lower surface of the wing. This can be seen for M=0. 835661, in figure 1, where there is a marked difference in pressure between tappings 3 and 3a. The theoretical curves on each –Cpvs x/c graph were designed using the Prandtl-Glauert law. As mentioned earlier, this law is based on thin aerofoil theory, meaning it is not exact and there are sometimes large errors between the proposed theoretical values and the experimental values achieved. These large errors are seen most clearly in the higher Mach numbers. This is because in the transonic range, where there is a mixture of sub and supersonic flow, local shockwaves occur and the theoretical curves do not take shockwaves into account. Hence, the theory breaks down when the freestream Mach number exceeds the critical Mach number for the aerofoil. At lower Mach numbers, the theoretical values line up reasonably well with those achieved through experiment. There only seems to be some error between the two, mainly arising in the 15-25% range. However, overall the Prandtl-Glauert law seems to be reasonably accurate as long as the Mach number remains sub-critical. The experiment itself was successful. The rough position of the shockwave and the critical Mach number were able to be identified. There are however some sources of inaccuracy or error that can be addressed of the experiment is to be repeated for ‘bettter’ results. Aside from the normal human errors made during experimentation the apparatus itself could be improved. Pressure tapping 1 (the closest to the leading edge) and pressure tapping 8 (the closest to the trailing edge) were placed at 6. 5% and 75% respectively. What this means is that they are not centralized relative to the leading and trailing edge effectively meaning it is not able to be determined whether or not the pressure is conserved. At a zero angle of incidence, the pressure at the tip of the leading edge should be equal to the pressure at the tip of the trailing edge. To improve this pressure tappings should exist at the LE and TE and possibly more pressure tappings across the aerofoil surface to provide more points for recording. Another source of improvement could be using a larger test section so that there is absolutely no disturbance in measuring the static pressure. However, this may only produce a minute difference in the data and may not be worthwhile for such little gain. Conclusion As desired, a symmetric aerofoil was tested in transonic flow and the experimental results were compared to the theoretical values predicted by the PrandtlGlauert law. In the cases where there was a large disparity between experimental and theoretical results, an explanation was given, relying on the theory behind transonic flow. Bibliography H. H. Hurt, J. (1965). Aerodynamics for Naval Aviators. Naval Air Systems Command. Mason. (2006). Transonic aerodynamics of airfoils and wings. Virginia Tech. Motallebi. (2012). Surface Pressure Measurements on an Aerofoil in Transonic Flow. London: Queen Mary University of London. How to cite Surface Pressure Measurements on an Aerofoil, Essay examples

Alzheimer’s Disease Samples for Students †MyAssignmenthelp.com

Question: Discuss about the Alzheimers Disease. Answer: Introduction Alzheimers disease is an irreversible and progressive disorder causing memory loss and disruption of other cognitive functions which severely interferes with daily life activities. It is the most common type of dementia and accounts for up to 75% of all dementia cases worldwide. It has been estimated that about 25 million people worldwide are affected by dementia of some kind (Qiu, Kivipelto von Strauss, 2009). The incidence of Alzheimers disease is strongly although not solely associated with ageing. The majority of affected individuals age above 65 years, however, early onset of Alzheimers is also been observed. There are more than 413,106 Australians suffering from dementia among which 55% are female and 45% male (Alzheimer's Australia | Statistics, 2017). With the world population ageing at a steady rate the frequency of dementia is expected to double by 2030 and hence is considered as a public health priority presently. Further, the global societal cost of Alzheimers disease is quite high, both in terms of direct burdens (medical and social care) as well as indirect burdens (unpaid caregiving by family and friends). This clinical update aims to address several aspects of the disease including prevailing diagnostic methods, distinction between different types of dementia, pathophysiology, prognosis and potential treatment options. Aetiology and Pathogenesis Scientists believe that Alzheimers is a multifactorial disease resulting from the culmination of a range of different factors, of which increasing age is the most potent risk factor of all. The strong association of the disease with old age is an indication of complex interaction of other risk factors such as genetic susceptibility, psychosocial factors, lifestyle and environmental factors experienced over the lifespan of the patient. Alzheimers is caused by brain cell death like all other types of dementia. Thus it is a progressive neurodegenerative disorder resulting in shrinkage of the overall brain size and decrease in nerve cells and connections between the same. Damage and changes to the brain start occurring from as long as a decade or more before the appearance of any clinical symptoms. Abnormal deposits of a protein called beta-amyloid causes amyloid plaques. Disintegration of another protein called tau tangles which as the name suggest tangles with different neurons of the brain. These beta plaques and tau tangles affects the normal functioning of the neurons and the neurons start losing neural connections (Swerdlow, Burns Khan, 2014). In the initial stages the hippocampus is only affected which is associated with memory functioning. In the later stages as the disease progresses other parts of the brain are affected and brain tissues shrink considerably (Fjell et al., 2014). However, the exact reason of why these plaques and tangles form and the onset of the disease mostly at an old age are still undiscovered. Researches provide several theories and age-related changes like mitochondrial dysfunction, inflammation, production of increased levels of free radicals, etc. which requires further investigation to treat and cure the disease. The disease progresses through three main stages namely Preclinical, Mild Cognitive Impairment and finally Dementia. During the preclinical stage no cognitive or memory impairment is observed, however changes in the brain tissue proceeds. In Mild Cognitive Impairment there are some signs disruption in cognitive functioning may appear but it does not interfere with normal daily activities of the patient (Vos et al., 2015). As the disease further progresses to severe cognitive impairment dementia and memory loss is observed. Several lines of risk factors are associated with Alzheimers. Table. 1 summarizes some of the established risk factors and protective associated with the disease. Aetiological Hypothesis Risk Factors/ Protective Factors Epidemiological Evidence Genetic Risk factors: APOE ?4 allele (Late-onset Alzheimers) Inherited genetic changes (Early-onset Alzheimers) Strong Vascular Risk Factors: Hypertension, high BMI, diabetes, Cardiovascular disorders, cerebrovascular disorders and smoking. Protective Factors: Light to moderate alcohol consumption, antihypertensive therapy. Moderate or Sufficient Psychosocial Protective Factors: High level of education, persistent cognitive and mental stimulating activities, increased social and physical activity. Moderate or Sufficient Nutritional and Dietary Risk Factors: Folate, Vitamin B12 and antioxidant deficiency. Protective Factors: Omega-3 fatty acids and vegetable consumption. Insufficient or Limited. Other (Toxic or inflammatory factors, etc.) Risk Factors: Head injuries, exposure to toxins and electromagnetic fields, depression and hormone replacement theory. Protective Factors: Non-steroidal anti-inflammatory drugs, Insufficient or Limited. Table 1: Risk and Protective Factors of Alzheimers Disease (Qiu, Kivipelto von Strauss, 2009) The public health impact of Alzheimers is profound. As the disease is costly in terms of both personal suffering and economic loss it has become an important facet of public health and health care delivery. Although the immediate clinical symptoms of the disease is limited to memory loss and other cognitive impairments, several non-cognitive secondary clinical features like behavioural disturbances, depression, disruption of daily life activities (Wimo et al., 2013). Several studies have estimated the financial burden of the disease by using self-report and observational tools. One study estimates the cost of the disease to be $38,000 per patient per year although estimates ranging from 50% lower to 50% higher have also been reported (Sloane et al., 2002). The main burden of care is upon informal caregivers. Time spent providing care ranges from 5.9 hours per week for patients with lower severity to 35.2 hours per week for patients with severe cognitive impairments and limitations (W ittenauer, Smith Aden, 2013). Hospitalization incurs the highest financial burden for patients with severe to moderate form of the disease. Clinical Manifestations Several signs and symptoms are associated with Alzheimers disease. Affected individuals may experience one or more of these symptoms to be diagnosed with the disease. Appropriate evaluation of the symptoms is essential for early diagnosis by medical practitioners. The symptoms often vary according to the severity of the disease i.e. mild, moderate and severe. Almost all the symptoms are related to memory and cognitions. Patients suffer from worsened ability to remember and process new information like conversations, appointments, navigations routes, etc. Impairments regarding reasoning, judgements and complex tasks such as inability to make appropriate decisions, manage finances or plan complex sequential activities. Vision is often affected in patients with Alzheimers disease causing moderate to severe visuospatial functioning impairments. Difficulty in reading, judging distances, determining colour, recognising familiar faces and objects and implementing tasks that involve some sor t of orientation are early symptoms of disease prognosis (Ismail et al., 2016). Further, behavioural changes are also extensively observed in Alzheimers patients. Mood swings, lack of interest and motivation, apathy, social withdrawal, compulsive and obsessive behaviour. Memory loss is the most common of all the symptoms and is associated with manifestation of all the other related symptoms. People are often diagnosed at mild stage of the disease which is most prominently characterised by mild cognitive impairment (Geda et al., 2013). At the initial stages it does not interfere with daily living activities but older people with the condition have higher risk of developing Alzheimers. As the disease progresses from mild to severe the brain ceases to work and the body shuts down. Diagnostic Processes Various guidelines for Alzheimers dementia and mild cognitive impairment can be used for general practice. To diagnose the disease the initial step is a medical assessment of the patient. Early diagnosis is crucial for providing appropriate treatment and intervention and restricts the prognosis of the disease as direct cure of the disease is yet to be discovered. A medical assessment should include examination of the patients family and medical history. Whether dementia runs in the family or any incidence relating to head injury can be high risk factors and might aid in early diagnosis. Physical examinations including measurement of blood pressure and other cardiovascular parameters must be performed to assess the effects of the same on progression of the diseased condition. Neurological tests like assessment of balance, sensory functions, reflexes, eye movements and other neurological functions may help in assessing the overall function ability of the patient and diagnose the diseas e. In the preclinical stage several biological and physiological changes are underway but no noticeable clinical symptoms are visible in the patient. Studies predict that the onset of this preclinical stage may begin years ever decades before any manifestation of the disease symptoms and hence diagnosis of this stage becomes somewhat difficult for medical practitioners and physicians. The diagnosis of this stage mostly depends on the identification of certain biomarkers that may signal the inception of these biological changes within the brain (Olsson et al., 2016). The most efficient biomarkers of Alzheimers disease brain imaging studies using biophysical techniques like magnetic resonance imaging (MRI), positron imaging tomography (PET) and estimation of several proteins present in the brain and cerebrospinal fluid. To assess mild and severe symptoms, established guidelines must be followed. Memory and cognitive skills, behavioural changes, degree of memory or cognitive impairment and the cause of symptoms are evaluated for such diagnosis (Hayne, Lim Donnelly, 2014). The practitioner must rule out other factors that can cause similar symptoms by thoroughly studying patient history. Parkinsons disease, depression, past strokes and other medical conditions must be considered prior to diagnosing the patient with Alzheimers disease. Treatment No drug has been formulated yet that can completely protect neurons from degenerative effects however pharmacological treatment primarily depends on inhibition of acetylcholine degradation in the nerve synapses. Acetylcholinesterase inhibitors are the only drugs that have been used to treat Alzheimers. They act by slowing down the process of degradation of neurotransmitters. Another group of drug, N-methyl D-aspartate receptor antagonist are also used that regulate the activity of glutamate and help in the proves of cell signalling. References Alzheimer's Australia | Statistics. (2017).Fightdementia.org.au. Retrieved 2 September 2017, from https://www.fightdementia.org.au/statistics Fjell, A. M., McEvoy, L., Holland, D., Dale, A. M., Walhovd, K. B., Alzheimer's Disease Neuroimaging Initiative. (2014). What is normal in normal aging? Effects of aging, amyloid and Alzheimer's disease on the cerebral cortex and the hippocampus.Progress in neurobiology,117, 20-40. Geda, Y. E., Schneider, L. S., Gitlin, L. N., Miller, D. S., Smith, G. S., Bell, J., ... Rosenberg, P. B. (2013). Neuropsychiatric symptoms in Alzheimer's disease: past progress and anticipation of the future.Alzheimer's dementia,9(5), 602-608. Hayne, D. J., Lim, S., Donnelly, P. S. (2014). Metal complexes designed to bind to amyloid- for the diagnosis and treatment of Alzheimer's disease.Chemical Society Reviews,43(19), 6701-6715. Ismail, Z., Smith, E. E., Geda, Y., Sultzer, D., Brodaty, H., Smith, G., ... Area, I. N. S. P. I. (2016). Neuropsychiatric symptoms as early manifestations of emergent dementia: provisional diagnostic criteria for mild behavioral impairment.Alzheimer's Dementia,12(2), 195-202. Olsson, B., Lautner, R., Andreasson, U., hrfelt, A., Portelius, E., Bjerke, M., ... Wu, E. (2016). CSF and blood biomarkers for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis.The Lancet Neurology,15(7), 673-684. Qiu, C., Kivipelto, M., von Strauss, E. (2009). Epidemiology of Alzheimer's disease: occurrence, determinants, and strategies toward intervention.Dialogues in clinical neuroscience,11(2), 111. Sloane, P. D., Zimmerman, S., Suchindran, C., Reed, P., Wang, L., Boustani, M., Sudha, S. (2002). The public health impact of Alzheimer's disease, 20002050: potential implication of treatment advances.Annual review of public health,23(1), 213-231. Swerdlow, R. H., Burns, J. M., Khan, S. M. (2014). The Alzheimer's disease mitochondrial cascade hypothesis: progress and perspectives.Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease,1842(8), 1219-1231. Vos, S. J., Verhey, F., Frlich, L., Kornhuber, J., Wiltfang, J., Maier, W., ... Frisoni, G. B. (2015). Prevalence and prognosis of Alzheimers disease at the mild cognitive impairment stage.Brain,138(5), 1327-1338. Wimo, A., Jnsson, L., Bond, J., Prince, M., Winblad, B., International, A. D. (2013). The worldwide economic impact of dementia 2010.Alzheimer's Dementia,9(1), 1-11. Wittenauer, R., Smith, L., Aden, K. (2013) Update on 2004 Background Paper Written by Saloni Tanna, Pharm.D. MPH Background Paper,6.