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6 DQ4 Essay

1. Compare independent variables, dependent variables, and extraneous variables. Describe two ways that researchers attempt to control extraneous variables. Support your answer with peer-reviewed articles. 2.Describe the “levels of evidence” and provide an example of the type of practice change that could result from each. 3.The theoretical foundations of qualitative and quantitative methods are very different, but many researchers believe both methods should be used in the research study to increase validity and reliability. What advantages or disadvantages do you see in using both types of methods in a nursing study? Support your answer with current evidence-based literature. 4.According to the textbook, nurses in various settings are adopting a research-based (or evidence-based) practice that incorporates research findings into their decisions and interactions with clients. How do you see this being applied in your workplace?

University of South Florida Mastery of Communication Skills Discussion

University of South Florida Mastery of Communication Skills Discussion.

I’m working on a management writing question and need a sample draft to help me learn.

Write 700-900 responding to the following prompts:What are the main things you learned about yourself from the five exercises you completed this semester?In three words (or short phrases), how would you characterize who you want to be as a leader?Is there a gap between who you are as a leader now and who you want to be? If so, what do you plan to do to address that?Who is a leader you admire and want to emulate? And why?
University of South Florida Mastery of Communication Skills Discussion

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help writing I need the same essay.

Question description Essay Questio nThe United states saw waves of immigration and several changes in immigration law from the mid-1860s to the late 20th century.PROMPT: The United States saw waves of immigration and several changes in immigration law from the mid-1860s to the late 20th century. Discuss the impact immigration, immigration laws, and the backlash to immigration had on the social and economic development of the United States. Consider ethical arguments and civics in your discussion of immigration and reaction to immigration. Also analyze change over time in your response. Hint: Think broadly here as you scattershoot/concept map your essay before writing. Start making a list of immigration related facts and primary sources to use in your response. Consider the impact of laws contracting and expanding immigration. Consider who the immigrants were in the various waves, where they went when they arrived in the US, and what they did when they got there. Consider also how immigrants influenced American society and culture and also why there was often a backlash to immigrants. Once you have jotted down your facts, choose the strongest points and supporting evidence to write your essay, making sure you address the prompt fully. Be sure to consider evidence from the entire time period of the prompt in your essay.Hint 2: Make sure that you integrate your discussion of Change over Time and Ethics/Civics throughout your analysis, not just in one paragraph. This means that Change over Time and Ethics/Civics WILL NOT be key points in your rule of three thesis statement.Requirements for the Signature EssayMust be in Rule of Three format with a introduction and strong thesis statement, 3 paragraphs of the body (each with their own thesis statement – one for each of the three key points of your overall thesis), and conclusion. So a minimum of 5 paragraphs.This is a fact based essay, you must provide specific and detailed evidence for your hypotheses.You must utilize a minimum of three primary sources from the assigned materials as evidence in your essayYou must utilize a minimum of three secondary sources from the assigned materials as evidence in your essayYou may only use materials assigned in this course for your essay (we have vetted all the materials utilized in this course, other materials may not be appropriate or accurate)DO NOT quote secondary sourcesYou may briefly quote a primary source (a phrase or a sentence) before immediately analyzing the relevance of the quote – a quote cannot stand alone as explanation or evidenceYou must consider change over time in this essayYou must consider ethics/ethical decision making in this essayYou must consider change over time in this essayDon’t forget about geography, where something takes place matters and it may be important to your argument.You must use Turabian citation style in this essay; all citations must be footnote style citations (no parenthetical cites allowed, no endnotes/works cited at the end, you need footnotes). Be sure to review how to properly cite a primary source that may be contained in another work and be sure to use page numbers where possible.12 pt type, 1 inch margins, double-spacedHow the Assignment is GradedThe assignment is worth up to 100 points. The following factors are taken into account when we grade:RULE OF THREE THESES – Do you have a well thought out and clear overall thesis in your introduction? Do you have a thesis statement for each of your three paragraphs of the body? Do the paragraphs of the body follow the overall thesis statement?EVIDENCE – You must have solid evidence for each point you raise in the thesis. Evidence is not simply a statement, there must be an explanation of how that evidence supports the thesis statement. Example: If you were writing a paragraph on the causes of the Cold War, you might use the Baruch Plan as an example. Simply writing “the Baruch Plan was a cause of the Cold War” in your paragraph would not be enough and would not be analytical. However, the following sentences do provide a good analysis of this piece of evidence:”One cause of the Cold War was the failure of the United States and the Soviet Union to agree upon a plan for nuclear disarmament after World War II. The Baruch Plan, presented by the US, would maintain the American atomic weapon advantage for the foreseeable future. This played into Stalin’s suspicions of the Americans’ true motivations toward the USSR.”Did you use the minimum number of primary sources? secondary sources?HISTORICAL ACCURACY, CLARITY, AND LOGIC Is your argument clear and does it make sense? Is it historically accurate? Does your evidence prove your point? Does your analysis answer the prompt? Have you considered change over time and geographic differences in your essay? PROPER CITATION Have you properly cited? Have you used Turabian/Chicago? You must also FOOTNOTE. Parenthetical cites are NOT allowed.GRAMMAR, SPELLING AND MECHANICSIs the essay up to college standards for grammar and spelling? Is it an analytical essay? Does it meet minimum length and formatting requirements?Textbook link https://cnx.org/contents/[email protected]:[email protected]/…
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Literature Review: Diabetes, Inflammation and Obesity

Literature Review: Diabetes, Inflammation and Obesity. LITERATURE REVIEW DIABETES The metabolic disease diabetes mellitus is marked by high blood glucose concentration as a result of impairment in insulin secretion and/or insulin action. The primary cause of high blood glucose concentration is most of the time not obvious as to be a result of either defects in insulin secretion or insulin action on target tissues since both impairments often occur in the same patient. Numerous factors may result in the formation of diabetes mellitus ranging from autoimmune destruction of the pancreatic β-cells leading to a decrease of insulin production to anomalies that cause insulin resistance. Impairment of insulin action on target tissues is the root of aberration in fat, protein and carbohydrate metabolism. The long-lasting effect of hyperglycemia in diabetics results in a range of organs to suffer from a decrease in function, long-term damage and failure. The organs being the most affected are the heart, eyes, kidneys, blood vessels and nerves. Chronic high blood glucose concentration may also result from growth impairment and vulnerability to certain infections (Diabetes Care 2004). There are two main types of diabetes; type 1 diabetes and type 2 diabetes. Type 1 diabetes is caused by a high decrease of insulin secretion while type 2 diabetes is caused by an amalgam of insulin resistance and an ineffective response to secrete more insulin to recompense (Diabetes care 2004). TYPE 1 DIABETES Previously called as insulin-dependent diabetes, type 1 diabetes is a consequence of cellular-mediated autoimmune destruction of pancreatic β-cells. Islet cell autoantibodies, antibodies to insulin, antibodies to glutamic acid decarboxylase (GAD65) and antibodies to the tyrosine phosphatases, IA-2 and IA-2β are markers for the immune destruction of the pancreatic β-cells. About 5-10% cases of diabetes are that of type 1 diabetes. This type of immune mediated diabetes is more pronounced in children and adolescence and at an advanced phase of this disease there is little or no insulin secretion (Diabetes Care 2004). TYPE 2 DIABETES Previously called as non-insulin-dependent diabetes, type 2 diabetes is probably bring about by many different causes which are yet not well known but is certainly not caused from autoimmune pancreatic β-cell destruction and insulin secretion is relatively deficient rather than absolutely deficient compared to type 1 diabetes. Type 2 diabetes is caused by insulin resistance and an ineffective response to secrete more insulin to compensate.. About 90-95% cases of diabetes are that of type 2 diabetes and it is more pronounced in adults and increases with age, obesity and insufficient physical activity. Unlike in type 1 diabetes, most patients with type 2 diabetes are obese and this obesity can cause further insulin resistance (Diabetes Care 2004). DIABETES STATISTICS In 2012, the estimated number of peoples with diabetes worldwide was more than 371 million out of which more than 4.8 million people died from this non-communicable disease (International Diabetes Federation 2012). This number has since increased in 2013 with more than 372 million people with diabetes worldwide out of which more than 5.1 million people died. According to International Diabetes Federation (IDF), in less than 25 years, the number of people with diabetes is estimated to go beyond 592 million (International Diabetes Federation 2013). As for Mauritius diabetes prevalence was 14.76% in 2012 (International Diabetes Federation 2012) and the same prevalence was recorded in 2013 (International Diabetes Federation 2013). Mauritius is no longer found in the top 10 countries/territories worldwide for prevalence of diabetes in 2013 (International Diabetes Federation 2013). It has been estimated that diabetic patients have two to four times more chance of dying from cardiovascular disease compared to non-diabetic patients (Gerich, 2007) and the main cause of death in people with type 2 diabetes mellitus is cardiovascular disease but also blindness, lower limb amputations and renal failure (King et al. 1998 and The Diabetes Atlas 2006). Among all the patients assigned with diabetes mellitus in Mauritius, about 40% died from heart disease and 30% from strokes (Ministry of Health and Quality of Life, 2011). There is also a high warning that diabetes may cause a major hindrance to global development according to latest figures (International Diabetes Federation 2013). INFLAMMATION IMMUNE SYSTEM The immune system is very diverse and helps to protect the body against infectious factors and the harm that they cause to the body as well as protection from other harmful substances like insect toxins (Kumar 2014 and Murphy 2012, p.3). The immune system is composed of many different types of effector cells and molecules and yet many more remains to be discovered since the study of immune system is relatively a new section of physiology and medicine (Kumar 2014 and Murphy et al. 2012, p.3). The immune system is classified into two major groups which are innate immunity and adaptive immunity and both innate and adaptive immune responses are dependent on the functions of white blood cells/leukocytes (Kumar 2014 and Murphy et al. 2012, p.4). Innate immunity consists of innate immune cells such as macrophages, dendritic cells, neutrophils, eosinophils, basophils, mast cells, platelets and natural killer cells and its humoral part, the complement system. Adaptive immunity consists of B-cell mediated humoral Immunity and T-cell mediated cellular immunity (Kumar 2014). When bacteria and other pathogens such as viruses, parasites and fungi cross the physical barrier such as the skin and/or chemical barrier such as the mucosal layer, the immune system comes into play to destroy the pathogens. Initially the first branch that comes into play is the innate immunity response. The pathogens are detected by the receptors on macrophages such as those found in tissues that attach to common constituents of several types of bacterial surfaces. Binding to these receptors cause the macrophage to engulf the pathogens as well as to digest it internally. Moreover, this binding also causes secretion of cytokines and chemokines which are proteins that transfer essential messages to other immune cells. Cytokines are any type of proteins secreted by cells and that alters the behavior of neighboring cells which have the suitable receptors. Chemokines are proteins that are secreted and function as chemoattractants which attract cells possessing chemokine receptors, such as monocytes (macrophage precursor) and neutrophils, from the bloodstream to the site of infection. The cytokines and chemokines secreted from activated macrophages begin the process called as inflammation (Murphy et al. 2012, p.10). INFLAMMATORY RESPONSE Infection triggers an inflammatory response. Inflammation is a helpful process to fight against infection through the use of proteins and cells from the bloodstream to the site of infected tissues resulting in the pathogens to be directly destroyed. The recruitments of those proteins and cells from the bloodstream are helped by cytokines which increase permeability of blood vessels. Moreover, an inflammatory response also causes more microbes and antigen-presenting cells to travel from the site of infected tissue to neighboring lymphoid tissues by increasing the lymph flow. The attraction of microbes and antigen-presenting cells into the lymphoid tissues are helped by chemokines and this cause the activation of lymphocytes and the stimulation of adaptive immune response. Furthermore, as soon as the adaptive immune response is activated, inflammation causes the mobilisation of the effector components of the adaptive immune response such as effector T-cells and antibody molecules to the site of infected tissues. Local inflammation and phagocytosis can also be activated as a consequence of the activation of a series of plasma proteins known conjointly as complement. The surfaces of bacteria lead to the activation of the complement system. This process causes the bacterial surfaces only and not the surfaces of own body cells to be layered with complement fragments through a series of proteolytic reactions. These complement-coated pathogens are then bound to specific complement receptors found on the surface of macrophages and neutrophils and eventually engulfed by phagocytosis and digested internally (Murphy et al. 2012, p.10-11). In the early phase of an inflammatory response, the main cell types that converge to the infected tissue sites are macrophages and large amounts of neutrophils followed by the convergence of monocytes to the infected tissues and there they swiftly mature into macrophages. In the later phase, if inflammation persists, the microbes are destroyed by the convergence of eosinophils in the inflamed tissues. Monocytes, macrophages, neutrophils and eosinophils are also called as inflammatory cells (Murphy et al. 2012, p.11). Inflammation is clinically named by the Latin words calor, dolor, rubor and tumor, which mean heat, pain, redness and swelling respectively. The increase in local blood flow and movement of fluid and blood proteins into tissues is due to an increase in blood vessels circumference and permeability respectively which caused the heat, redness and swelling and ultimately this process is caused by the effect of cytokines. Pro-inflammatory cytokines which are produced by endothelial cells in response to an infection alter the stickiness of endothelial cells, inducing mobile leukocytes to adhere to and pass in between the endothelial cells to the infected tissue sites attracted by chemokines (Murphy et al. 2012, p.11). Examples of those adhering molecules that helps leukocytes to pass in between the endothelial cells are selectins (E-selectin, P-selectin), cell adhesion molecules [intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1)], and integrins (Devaraj et al. 2008). The movement of leukocytes in between the endothelial cells and their action is what cause pain (Murphy et al. 2012, p.11). C-REACTIVE PROTEIN Examples of pro-inflammatory cytokines that are released by macrophages during an infection are the molecules tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and iterleukin-6 (IL-6). These molecules have an important function in triggering an acute-phase response in the liver and to trigger fever also (Murphy et al. 2012, p.98-101). The liver cells, hepatocytes, are operated by these cytokines in the acute-phase response and the hepatocytes react by altering the profile of proteins that they produce and release into the bloodstream, where the blood levels of some proteins decreases while others increases. The proteins that are produced and secreted only by the action of TNF-α, IL-1β and IL-6 on hepatocytes and that have also a similar effect like antibodies are referred as acute-phase proteins (Murphy et al. 2012, p.109). C-reactive protein (CRP) is an acute-phase plasma protein (Black et al. 2004) and is formed from five identical subunits, thus forms part of the pentraxin protein family (Murphy et al. 2012, p.110). BIOLOGICAL FUNCTIONS OF CRP C-reactive protein is also a multipronged pathogen recognition molecule. It adheres to the phosphocholine unit of some bacterial and fungal cell-wall lipopolysaccharides (LPS), such as pneumococcal C polysaccharide, therefore the name C-reactive protein (Murphy et al. 2012, p.56, 110). However, C-reactive protein cannot bind to the phosphocholine unit of mammalian cell membrane phospholipids. When C-reactive protein adheres to a bacterial cell wall, it makes the bacterium more susceptible to phagocytosis (act as an opsonin) and it also turns on the complement cascade by adhering to C1q, the first molecule involved in the complement system activation (Murphy et al. 2012, p.110). EPIDEMIOLOGY OF CRP C-reactive protein is a non-specific and very stable used marker for acute inflammatory processes (Anzai et al. 1997 and Paffen and deMaat 2006). Several evidences has put forward that the levels of the biomarker of inflammation, C-reactive protein, is linked with several problems related to cardiovascular diseases (Bisoendial et al. 2010) such as acute myocardial infarction, unstable angina pectoris (Lagrand et al. 1999), atherosclerosis (Libby and Ridker 2004), atherothrombosis (Pepys and Hirschfield 2001) and also hypertension (Sesso et al. 2003). However, there have also been reports on no relationship between C- reactive protein and myocardial infarction after establishment of risk factors associated with cardiovascular diseases such as smoking and age (Doggen et al. 2001). High levels of C-reactive protein have also been linked with diabetes (Calle and Fernandez 2012) and obesity (Tracy et al. 1997). INFLAMMATION, OBESITY AND DIABETES Chronic inflammations, whereby higher levels of inflammatory markers such as tumor necrosis factor-α and interleukin-6 occur have been linked with metabolic disorders (Fasshauer and Paschke 2003). It has been observed that the innate immune system of obese peoples is often activated and this cause a low-grade inflammation of white adipose tissue and subsequently make an increase in the level of certain biological markers of inflammation such as C-reactive protein, tumor necrosis factor-α and interleukin-6 (Bastard et al. 2006). The innate immune cells contain receptors on their surfaces that identify molecular prototypes present on pathogens known as pattern-recognition receptors (Cawthorn and Sethi 2008). One of the most well known pattern-recognition receptors is the toll-like receptors (TLR) such as TLR2 and TLR4 that can identify fatty acids and trigger the production of pro-inflammatory cytokines by macrophages (Murphy et al. 2012, p.85-86 and Shi et al. 2006). Upon binding of the molecular prototype of pathogens and pattern-recognition receptors, nuclear factor-kappa-B (NF-kB) signaling pathways are triggered resulting in an inflammatory response (Cawthorn and Sethi 2008). Low-grade inflammation can consequently give rise to diseases such as insulin resistance, impaired glucose tolerance and also diabetes (Bastard et al. 2006). According to a study done by Barzilay et al. (2001) it has been found that obese peoples with higher C-reactive protein levels have two times more risk of having type 2 diabetes within three to four years. Insulin sensitivity is altered in many different ways through changes in different steps of the pathway of insulin signaling (Calle and Fernandez 2012). One of the many steps alteration include the phosphorylation of the serine residues of the insulin receptor substrate-1 (IRS-1) rather than the tyrosine residues due to elevated levels of tumor necrosis factor-α and interlukin-6. This causes the cessation of insulin signaling thus causing insulin resistance (Fasshauer and Paschke 2003). Moreover, the phosphorylation of serine residues of the insulin receptor substrate-1 can also be caused by high levels of free fatty acids (FFAs) which cause elevated inflammation by activation of toll-like receptors and activation of Jun N-terminal kinase (JNK) thus leading to type 2 diabetes (Hotamisligil 2008). In turn, hyperglycaemia triggers iterleukin-6 production from endothelium and macrophages but also stimulates the action of suppressor of cytokine signaling (SOCS) therefore exacerbating insulin resistance (Rønn et al. 2007). Literature Review: Diabetes, Inflammation and Obesity

How Your Self Assessments Impact Your Personal Life Discussion Paper

How Your Self Assessments Impact Your Personal Life Discussion Paper.

after viewing the interactive discussion scenario, answer the question(s) posted at the end of the presentation.A transcript for the video is available here.To complete this assignment, review the Discussion Rubric document. PART 2 In your learning journal, reflect on how your self-assessments impact your personal life.Recap the results you achieved on each assessment.Did anything surprise you? Did you share any of the results with family or friends?What did you learn about yourself as a learner from doing the assessment, and how will you incorporate this into the rest of this course and the remainder of your education?THE LINK TO THE VIDEO AND THE SELF- ASSESMENT RESULTS WILL BE SEND TO YOU .
How Your Self Assessments Impact Your Personal Life Discussion Paper