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Global societal problem

Identify the global societal problem within the introductory paragraph.
Conclude with a thesis statement that states your proposed solutions to the problem.
Describe background information on how that problem developed or came into existence.
Show why this is a societal problem.
Provide perspectives from multiple disciplines or populations so that you fully represent what different parts of
6/23/22, 7:05 PM Writers Hub – Freelance Writing
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society have to say about this issue.
Construct an argument supporting your proposed solutions, considering multiple disciplines or populations so
that your solution shows that multiple parts of society will benefit from this solution.
Provide evidence from multiple scholarly sources as evidence that your proposed solution is viable.
Interpret statistical data from at least three peer-reviewed scholarly sources within your argument.
Discuss the validity, reliability, and any biases.
Identify the strengths and weaknesses of these sources, pointing out limitations of current research and
attempting to indicate areas for future research. (You may even use visual representations such as graphs or
charts to explain statistics from sources.)
Evaluate the ethical outcomes that result from your solution.
Provide at least one positive ethical outcome as well as at least one negative ethical outcome that could result
from your solution.
Explain at least two ethical issues related to each of those outcomes. (It is important to consider all of society.)
Develop a conclusion for the last paragraphs of the essay, starting with rephrasing

Sample Solution

ling pathway activation [REF Tabas I. 1997 & 2002 4,5]. It is therefore that the majority of the cholesterol found in the body exists in its more stable, less cytotoxic, esterified form (cholesteryl esters (CE)) that take up about 2/3 of the serum cholesterol. Lecithin-cholesterol acyltransferase (LCAT) drives the esterification of a FC molecule in plasma, adding a single fatty acid to the hydroxyl group [REF 6 glomset 1968]. The conversion of un-esterified cholesterol towards CE enables cells to store and transport cholesterol, without the risk of FC induced cytotoxicity [REF]. Upon hydrolyzation by cholesteryl ester hydrolase, cholesterol and free fatty acids are regained for further biosynthesis [REF 36 goedeke]. Besides the eminent role in animal cellular membrane modulation, cholesterol influences a range of pathways i.a. as the precursor for hormone steroidogenesis [REF] and bile acids [REF], plays a significant role in transmembrane signalling [REF] and cellular proliferation [REF fernandez 7]. Despite the functional diversity between cholesterol using pathways, acquisition of cholesterol follows, for most mammalian cells, a comparable pattern. Cellular cholesterol is either de novo synthesized or derived from exogenous uptake from the circulation. 3 LIPID METABOLISM 3.1 DE NOVO SYNTHESIS OF CHOLESTEROL De novo synthesis of cholesterol is mainly found in vertebrates and in low amounts in plants, (not in prokaryotes) [REF Behrman EJ, 2005 8] and derived via the mevalonate (MVA) pathway. The MVA is a fundamental metabolic network providing essential elements for normal cellular metabolism and executed in the endoplasmic reticulum (ER) and cytoplasm of a cell. Despite the presence of MVA pathway in almost all animal cells, the contribution per organ differs. The human brain generates vast amounts of de novo synthesized cholesterol, approximately 20% of the total cholesterol pool and primary FC, mainly found in myelin sheaths that insulate axons [REF dietschy turley 2004 9]. Moreover, the hepatic contribution to the cholesterol pool derived from de novo synthesis varies per species, hepatic cells in mice contribute approximately 40% to the whole cholesterol synthesis, while human liver cells adds only 10% to the total pool [REF Dietschy turley 2001 10 REF 30 Goedeke ]. The MVA-pathway is a highly controlled enzymatic process, resulting in the stepwise formation of FC [REF reviewed by 11 tricarico 2015 16067-16084]. The newly formed cellular cholesterol is either directly used as a precursor for metabolites (bile acids, steroids, water soluble vitamins, included in the membrane) or converted towards CE by acyl-Co A acyl transferase (ACAT) and either effluxed towards the plasma compartment or stored in lipid droplets [REF 12 35 goedeke]. The stored CE within lipid droplets can be converted into FC by hormone sensitive lipase (HSL)[REF]. Since appropriate cellular cholesterol levels are critical for normal cell metabolism, the regulation of intracellular cholesterol levels are tightly controlled by feedback m
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