Difference Between Bank Credit Risk And Bank Capital Risk

1. Explain the difference between bank credit risk and bank capital risk The credit risk is the risk that promised cash flows from loans and securities held by FIs may not be paid in full (T). Capital risk is a more broad concept. The capital risk can be defined as the risk that a company will lose their investment (FFD), which means any investment with risk will take on capital risk to the investors. Moreover, the capital risk can also be regarded as the risk that an FI may not have enough capital to offset a sudden decline in the value of its assets, which amount to the insolvency risk. The main difference between these two risks is that they caused by different situations and they are two different behaviors decide their degrees. For†¦show more content†¦Capital risk relates to the ability to absorb losses, losses can be incurred due to credit risk, liquidity risk etc. However, credit risk is the probability that the borrowers will default on paying the money back. High credit risk can bring about insolvency risk, and high insolvency risk are likely to lead to bank’s bankruptcy. Thus, capital risk will exert more direct impact on banks than credit risk. There are three main types of individual consumer lending, which are housing loan (residential mortgage loan), revolving loans and fixed term personal loans. According to the data definition of the Bankscope, residential mortgage loan is a loan that secured by residential property. A loan provided by credit cards can be regarded as a revolving loan. People who have a revolving loan ca n draw and repay up to an amount of money in the life of the loan contract. In contract, fixed-term personal loans is credit that cannot be used again after payment. Once finished all of the payment, the borrower would no longer owe money and cannot draw any money. Purpose for purchasing is the main difference between housing loan and revolving loan. Housing loans have specific purchasing purpose, borrowers only can use the loan to purchase their houses. Nevertheless, people with revolving loan, for example the credit card, are able to purchase anything within the line of credit. The second difference is that residential mortgage loan must need

The Trail Of Tears American History - 1631 Words

When people hear about the Trail of Tears, the only thought to really pop up in their mind is a bunch of Indians died while being forced to emigrate from their homes. Many people believe that the Trail of Tears revolves only around the Cherokee Indians because the name came from their language. Of the Cherokee who made it to the west without death taking them, they called this forced removal, â€Å"Nunna Daul Isunyi—The Trail Where We Cried† (Langguth, 311). The Trail of Tears is a blackspot on American history; it is purposely brushed over quickly in American classrooms. This event encompasses so much more than what young Americans are taught. The tribes put on these trail went through punishing trials; multiple diseases, insufficient resources, extreme weather, and finally death from being starved and fatigued. There were countless tribes affected, emigrated, and annihilated by white settlers such as the Seminoles, Choctaws, Creeks, Chickasaws, and Cherokees; it was t he final chapter for natives in the east. It can be said that the ruin of the Native Americans started as far back as when the first settlers landed in North America. The main progression of their forced emigration, however, was due to the War of 1812. A professor of history, David Koch states, â€Å"There is no question, the alliance with the English destroyed any slim chance the natives might have had to retain any lands in the east.† (Bulletin, n.p). The War of 1812 is seen as a step in the United States’Show MoreRelatedTrail Of Tears Essay1649 Words   |  7 PagesThe Trail of Tears is part of the immoral history of the United States. The information in this paper will be about the causes, history, deaths, and the hopes that were lost. There were at least four causes for the Indian removal act of 1830. The history of the trail discussion about the Native Americans, and what happens to them when they were moving to their new home in the west, as well what happened after the removal act. The main causes of why the Native Americans had to be removed will beRead MoreAmerican History: Native Americans 829 Words   |  3 PagesHave you ever wondered what it would be like to be Native American during the European invasion? In American history Native Americans were treated unfairly. The American government mistreated the Natives by lying to them and treating them as foreigners. After years of fighting for freedom the Natives did not achieve their goal for freedom. The Trail of Tears, being the most tragic event in American history, was due to the Removal Act in the 1830s, the misguidance of President Andrew Jackson, theRead MoreTrail of Tears1191 Words   |  5 PagesTitle of the Lesson: Trail of Tears Content Area(s): Social Studies, Literature, Technology Unit of Study: Trail of Tears/US History Grade Level: 4-6 Time Frame: Comprehensive Unit/Lesson scheduled to take 3 weeks including reading of novel and a few different projects NCSS Themes: 1. Culture, 2. Time, Continuity and Change 3. People, Places Environment 4. Individual Development and Identity 5. Individuals, Groups, and Institutions 6. Power, authority, and governance Standards: Read MoreEssay on The Cherokee Trail of Tears1035 Words   |  5 Pagesnew problems. Native American Indians lived in peace and harmony until European explorers interrupted that bliss with the quest for money and power. The European explorers brought with them more people. These people and their descendants starting pushing the natives out of their homes, out of their land, far before the 1800s. However, in the 1800s, the driving force behind the removal of the natives intensified. Thousands of indians during this time were moved along the trail known as Nunna dual TsungRead MoreThe Trail Of Tears By James Collins1452 Words   |  6 PagesJames Collins Donald West History 201 December 1, 2015 TRAIL OF TEARS The trail of tears is also referred to as the period of Indian s removal. It was a period where Native Americans in the U.S were forcefully relocated following the removal of Indian Removal Act of 1830. Those who were forcibly moved were from Cherokee, Muscogee, Seminole, and Chickasaw and Choctaw nations in the southern U.S, an area initially referred to as the Indian Territory. Migration from Cherokee nation had begun in theRead MoreThe Trail Of Tears : The Rise And Fall Of The Cherokee Nation1106 Words   |  5 PagesMost Americans have at least some vague image of the Trail of Tears, but not very many know of the events that led to that tragic removal of several thousand Indians from their homeland. Indian lands were held hostage by the states and the federal government, and Indians had to agree to removal to preserve their identity as tribes. Trail of Tears is an excellent snapshot of a particular situation and will be eye opening to those who are not familiar with the story o f the southern tribes and theirRead MoreThe Trail Of Tears : The Rise And Fall Of The Cherokee Nation1315 Words   |  6 Pages Most Americans have at least some vague understanding of the Trail of Tears, but not many know about the events that led to that tragic removal of thousands of Indians from their homeland. Indian lands were held hostage by the states and the federal government. The Indians had to agree to removal to maintain their tribe identities. Trail of Tears is an excellent example of a particular situation and will be eye opening to those who are not familiar with the story of the southern tribes and theirRead MoreThe Impacts Of A Cherokee Story : Trail Of Tears920 Words   |  4 PagesStory: Trail of Tears One of the major atrocities early in the United States (US) expansion came after President Andrew Jackson approved of and signed the Indian Removal Act in 1830. This document set the foundation for what would be known as the Trail of Tears. The Trail of Tears was the forceful relocation of give main Native American tribes from their eastern lands, to newly established territories located west of the Mississippi River (Dwyer, 2014, p. 33). After researching the Trail of Tears’Read MoreStarvation, Illness and Death of the Native Americans in Trail of Tears1352 Words   |  6 PagesOne of the greatest injustices of American history included, starvation, illness, and death. These hardships were undeservingly forced upon an innocent group of people – the Native Americans. One may think that the Trail of Tears was only a simple journey the Indians made to discover new frontiers. This is not the case. The Trail of Tears was the result of the white man’s selfishness , causing Indians to lose their homes and belongings. The act was full of unfair treatment, cruelty, and heartlessnessRead MoreMost People Can Not Imagine Having To Walk 1000 Miles Across1211 Words   |  5 Pages during the Trail of Tears and the Holocaust, these awful imaginings were reality. Because the Nazis did not want eyewitnesses, most prisoners were regularly gassed, and less than 20 of the several thousand survived. Some prisoners buried their testimony in jars before their deaths, allowing the world to hear their story. This desire to â€Å"hide† the unthinkable did not just happen with the Holocaust, however; it also happened in the Trail of Tears, when all evidence of Native American culture was all

Why Search Engines and Databases Produce Different Types of Results Free Essays

Living in the Information Age (SOS-110-OL) Writing Assignment 2 The difference between what evaluative and assessment information is provided by an Internet search using Google. com and a search using EBSCO’s Academic Search Premier Database is extremely different. I started my searches by open two different internet windows, Google on one and EBSCO on another. We will write a custom essay sample on Why Search Engines and Databases Produce Different Types of Results or any similar topic only for you Order Now My Google search and EBSCO search was â€Å"articles on privacy and security on the internet†. The top result from Google was ftc. gov. This page had a list of three different microsites, two did not have any articles and the other one did. The article I found was on Malware. When I evaluate this article from the techniques from the Berkeley site, it does not rate well. It has no author and it does not cite any sources. The one plus it does have is that it is from a . gov site. Even though it does not rate well I do trust this site. The reason why I trust the site is because in the fifth step of the evaluation process, listen to your gut reaction. Think about why the page was created, the intentions of its author. My gut reaction tells me the information is coming from a government cite so I trust it. The purpose of this article was to inform and educate, there were no other intentions other than to inform and educate. My top result from EBSCO was an article from Communications of the ACM called Privacy and Security as Simple as Possible, But Not More So. The authors of this article are very creditable and qualified on the topic. This article was published to inform, give facts and some opinion. The article’s sources are document with footnotes throughout. Overall, this is a credible and useful source of information. It as creditable authors and all of the information was backed up with creditable sources. Like I said earlier the difference between what evaluative and assessment information is provided by an Internet search using Google. com and a search using EBSCO’s Academic Search Premier Database is extremely different. Search engines locate web pages that contain the keywords that the users entered. They also can find articles but it can be difficult to narrow down results. Like the search I just completed â€Å"articles on privacy and security on the internet† the search engines finds web pages not articles, so most of the information that came back from the search did not really pertain to what I was looking for. The database search on the other hand searched for actual articles that pertained to the subject that I was looking for, it is more organized and easier to access. Database much like the internet have massive amounts of data in which they can pull information but databases mainly will pull their articles from newspapers, magazines, journals and electronic reference sources so it is a more creditable source. Internet search engines and database searches can both provide good sources of information when doing searches. I found that the database search was more organize and had more information that pertained to my subject. How to cite Why Search Engines and Databases Produce Different Types of Results, Papers

Chronic and Acute inflammation

Questions: 1. Talk about Inflammation and distinguishing between Chronic and Acute inflammation (with examples). 2. Explain more details about chronic inflammation (with examples).Explain Causes of Chronic inflammation especially lifestyle, diet lack of exercise, obesity life-stress, genetic etc.explain how lifestyles affect the cause of chronic inflammation. 3. Talk about Chronic inflammation associated diseases and treatments eg T2D. Atherosclerosis-cardiovascular, cancer. 4. Components of Chronic Inflammation, Types of inflammatory cells and mediators, Neutrophils, macrophages or monocytes, mechanism of macrophage activation or polarisation. Answers: 1. Inflammation Inflammation is referred to the localized physical condition where due to some physiological reactions, the body parts become reddened, hot, swollen and painful. Usually, these kinds of phenomenon results from the infection, external or internal injury (Aggarwal et al. 2012). The process is a part of complex biological response of body tissues towards the harmful stimuli including damaged cells, pathogens or irritants. Through these kinds of processes, the immune cells protect body system by involving different immune cells, blood vessels and molecular mediators. Through this process, the immune cells eliminate the initial causes of cell injury by clearing out the necrotic and damaged tissues from body and promote the tissue repairing system. Its five basic signs, calor or heat, dolor or pain, rubor or redness, tumor or swelling and loss of function characterize the phenomenon, inflammation. It is the initial response of immune system and mediated by the immune cells, thus, it is classified under the innate immunity or cell mediated immunity in comparison to the adaptive immunity that is specific for each pathogen. There are mainly two types of inflammation which are acute and chronic inflammation (Cho and Yu 2012). Chronic inflammation is more severe form of inflammation than the acute one. Acute inflammation Acute infection is usually induced in the damaged tissues as a result of trauma, microbial invasion or noxious compounds. The acute inflammation is mediated by the immune cells and the secreted chemical mediators, which are known as cytokines and other molecules. In the case of acute inflammation, the anaphylatoxins are released at inflammation site, which are small inflammation-causing chemicals, these mediators promote the secretion of chemical mediators including histamine, prostaglandins or serotonin from the mast cells, thereby causing blood vessel expansion, making them more permeable (Daniluk 2012). In this way, the neutrophils are allowed to migrate into the affected tissue through diapedesis for clearing out the noxious substances in blood. The more blood cells accumulation causes redness and the destructive reactions cause heat. Most of bacterial or fungal infections cause acute inflammation. Lesions include pus, rash and abscess. For example, allergic anaphylaxis causes ac ute inflammation (Dietert and Luebke 2012). Chronic inflammation In contrast to the acute inflammation, the chronic inflammation is seen as a response to some viral infections and hypersensitivity reactions. It is seen in some infections where the inflammation is persistent. In contrast to the neutrophils and chemical mediators released by mast cells, the primary immune cells are T lymphocytes and macrophages here. The cytokines secreted by these cells causes more long-term damage to the tissues (French 2011). In the case of chronic inflammation, the acute infection allows continuous tissue damage to cells leading to tissue fibrosis. Lesions include fibrosis, rash or granuloma. Example includes autoimmune condition such as rheumatoid arthritis. 2. Chronic inflammation Chronic inflammation is usually the persistent and ongoing inflammation process after an acute inflammation. If the infection persists with more tissue destruction after the phase of acute inflammation, it can be said that chronic inflammation has taken place. In some cases, some pathogens directly provoke chronic inflammation in spite of initiating an acute inflammation first. Increased permeability of capillaries, increased blood flow and many other factors of acute inflammation continue with chronic stage (Lichti 2012). Neutrophils enter into the infected tissue and quickly recruit lymphocytes and macrophages through chemical mediators secretion. Macrophages initiate the phagocytosis process. Sometimes, they are not able to digest all the engulfed material and the pathogenic substances persist within macrophages while the macrophages are engulfing more, thereby continuing the symptoms of inflammation for longer period. In some cases, macrophages fuse and forms giant cells and thes e fused cells are found in the form of layers surrounding the damaged central core, which are known as granuloma. It is one of the significant features of tuberculosis (Ashton Acton 2012). Causes of Chronic inflammation There are a number of causes, which could cause chronic inflammation. Lifestyle Sedentary lifestyle, stress and exhaustions are crucial cause of chronic inflammation. Consuming a huge number of antibiotics can cause inflammatory symptoms via cross-reaction. More exposure to toxin for example, farmers working with pesticides can cause chronic inflammation. Vitamin D is an important component of system modulation, lack of sun exposure lowers the immune systems ability to work properly, enhancing chance of inflammation (Roy et al. 2012). Diet There are a number of foods, which can cause inflammation. Sugar triggers a number of cytokines causing inflammation. Saturated fat is another food substance, which cause inflammation of adipose tissues. Thus, cheese, full-fat dairy products, grain-based desserts, red meat should be avoided in diet. Trans fat causes systematic inflammation. Gluten and casein are also causative agents of chronic inflammation. Thus, food substances containing these factors should be avoided from daily diet. Alcohol and smoking are also major causes of inflammation (Schillde 2013). Lack of exercise People having insomnia are prone to chronic inflammation due to over secretion of inflammation causing cytokines. Lack of sleep promotes inflammation. Individual experiencing autoimmune disease are seen to have less sleep which promote the situation with more pain. Exercise helps to active the immune system. Exercise causes healthy muscle contractions, which causes the secretion of cytokines like IL-6, IL-8 and IL-15, thereby contributing in anti-inflammatory actions (Wick and Grundtman 2012). Obesity and depression Macrophages infiltrate the adipose tissues and release another set of chemical mediators which further promote inflammation. It has been reported that the accumulation of macrophages also causes insulin resistance in obese people. In addition, evidence suggest that depression and stress has a significant link with chronic inflammation. At stressed condition, more cortisol hormones are produced which is also promoted to the cytokines released due to lack of sleep that is interconnected with stress. These are stimulators of chronic inflammation (Thilakarathna and Rupasinghe 2013). Genetic Acute inflammation is followed by chronic inflammation signs through the signal transduction. JAK-STAT pathway has a major role in signal transduction. Mutation in these pathways can cause inflammation. Some autoimmune diseases are also caused by mutation in essential genes. 3. Chronic inflammation associated disease and treatments Type 2 Diabetes As described earlier, accumulation of macrophages at the site of inflammation has a major role in causing insulin resistance, which is the major cause of type 2 diabetes disease. Researchers found that accumulated macrophages secretes some immune mediators including TNF-alpha and other cytokines which are promoting the expression of some proteins which suppresses the insulin-signaling pathways, thereby making the system less responsive towards insulin and thereby loosing the control over glucose metabolism. It promotes the development of type 2 diabetes. FOXO 1 increase cytokine secretion, which has been shown to be more active during insulin resistance (Garca-Lafuente et al. 2009). Avoiding sugar and saturated fat based food is the basic treatment of type two diabetes to reduce the chance of diabetes. Sulforaphane has been shown to have great response as an anti-inflammatory activity while acting against oxidative damage associated with inflammatory activities. Atherosclerosis-cardiovasculardisease Atherosclerosis is a syndrome, which affects the blood vessels as a result of chronic inflammatory responses of WBCs present in the artery walls. The process is promoted by the LDLs as a result of failure of removing fats and cholesterol by the HDLs from macrophages. The result is formation of atherosclerotic lesion in artery, which is the cause of cardiovascular accident (Kawasaki et al. 2012). The retention of LDL particles promotes initial damage to vessel walls which promote inflammatory procedure. Macrophages further ingest oxidized LDLs and turn into foam cells which propagate the inflammatory process. In the case of cardiovascular diseases, atherosclerosis is the major cause. High blood pressure, smoking, high cholesterol, all of these inflammatory phenomenon triggers cardiovascular diseases. The damage promotes inflammatory response and leads to the formation of plaque in artery. Two types of plaques are formed in the cardiovascular diseases as a result of inflammatory responses. Stable plaques in artery of heart cause chest pain and sudden rupture of plaque causes blood clot and myocardial infarction (Gentile et al. 2012). Regular exercise and cessation of smoking are basic treatment. Combined treatment strategies are best for these cases. Lipoprotein transport behaviors have been shown successful results. Mediterranean diet can improve the symptoms. Medications for reducing high cholesterol can be a good treatment along with dietary improvement. Cancer A number of inflammatory diseases increase the risk of cancer of an individual. For example, it has been found that chronic inflammatory bowel disease increases the risk of colon carcinoma. Bacterial, viral or parasitic infections or chemical irritants can cause chronic inflammation. Through the inclusion of proneoplastic mutation, apoptosis, adaptive responses the inflammatory mediators promote neoplasia (Guo et al. 2012). As much the inflammation persists, the risk of cancer increases. In this context, anti-inflammatory medications and healthy diet by avoiding inflammation-inductive foods can be helpful. 4. Components of chronic inflammation Inflammation mediators There are different chemical and biological mediators of chronic inflammation, which are important components of chronic inflammation. Cytokines are the most important agents having significant role in inflammation. The cytokines, which promote inflammation, are known as the pro-inflammatory cytokines, which involve IL-6, IL-8, IL-15, TNF-alpha. The chemical mediators of inflammation include histamine, postraglandin, bradykinin and serotonin. Histamine is one of the initial chemical mediators released from mast cells which attracts macrophages at the site of inflammation (Mathur and Pedersen 2009). Neutrophils Neutrophils are most abundant granulocytes having a major role in inflammation process. These are the first leukocytes, which are recruited to the site of inflammation. They are able to eliminate the pathogens through phagocytosis. These cells have high capacity of infiltrating in the damaged tissues. These cells have a significant role in the chronic inflammation of joint. The granules in neutrophils secrete anti-microbial substances including toxic oxygen metabolites. And drive inflammation through antigen presentation and cytokine secretion. These are found in rheumatoid joints in large amount (Guo et al. 2012). Macrophages Monocytes are one of the important white blood cells. Monocytes migrate in different tissues while differentiating into macrophages. In inflammation, the macrophages has three major roles, phagocytosis of pathogenic substances, antigen presentation to the T lymphocytes and immunomodulation by producing and secreting different cytokines and growth factors. The chemical mediators secreted by the neutrophils make the macrophages active and these macrophages can infiltrate tissues easily. Activated macrophages can destroy the pathogens by phagocytosis more vigorously (Sica and Mantovani 2012). Mechanism of macrophage activation or polarization M1, M2 and M3 polarization Macrophages play an essential role in regulation of the process of healing of wound and regeneration of tissue by changing their state of polarization in response to the stimulus of local microenvironment. The native roles of macrophages that are polarized includes the needs of tissue remodeling and biomaterials, yet directing the response of polarization has been mainly not present as a probable strategy to use in regenerative medicine up till now (Herder et al. 2015). The macrophages that are derived from the precursors of monocyte go through specific differentiation depending on the environment of local tissues. They give response to the environmental signals within then tissues such as the activated lymphocytes, microbial products and damaged cells to distinguish into functional phenotypes. The phenotype of M1 macrophage is differentiated by the production of elevated levels of pro-inflammatory cytokines, capacity to mediate resistance against pathogens, high production of reacti ve intermediates of oxygen and nitrogen, strong microbial properties and promotion of responses of Th1. On the contrary, the M2 macrophages are differentiated by their involvement in the process of remodeling of tissue, parasite control, and regulation of immune system. Kappa (NF-KB) is a nuclear factor, which acts as a signaling molecule in the M1, M2 and M3 Polarization (Herder et al. 2015). 5. THP-1 cell model This model encompasses human leukemia monocytic cell line that has been widely utilized to study the mechanisms, functions, pathways of signaling and transport of drugs and nutrients involved with macrophages/monocytes. This model encompassing the cell line has become widespread for estimating the modulation of the activities of macrophages and monocytes (Qin, Z., 2012). THP-1 is a human monocytic cell line, which is derived from the patient suffering from acute monocytic leukemia. This cell line is utilized for the testing the cell lines of leukemia immunocytochemical analysis of protein-protein interaction and immunohistochemistry. These cells have C3b and Fc receptors and they are devoid of cytoplasmic and surface immunoglobulins. They are responsible for the production of IL-1 and stain positive for alpha-napthyl butyrate esterase. They exhibit increased production of carbondioxide during phagocytosis and can be distinguished into cells, which are like macrophage (Chanput et al. 2014). Strengths and Limitation In the present settings of research, THP-1 model is extensively used for the investigation of regulation and function of macrophages and monocytes in the cardiovascular system. In the studies, associated with the interaction between a variety of vascular cells and THP-1 cells, THP-1 cells offer several exceptional values like a model for investigating the mechanisms of the different stages of atherogenesis (Chanput et al. 2014). A few studies that are associated with the transcriptome, histone modification of THP-1 cells and microRNA profile, a number of molecules have been identified which may play crucial roles in regulating the macrophages and monocytes under pathological and physiological conditions. The limitation of this model is that there are noteworthy differences between the primary monocytes-macrophages and THP-1 cells and it is necessary to identify the differences between them. Moreover, both of them have diverse pathophysiological processes in programmed cell death or a poptosis (Qin, Z., 2012). Advantage and disadvantage of THP-1 cells over other cell models THP-1 cell line has some technical advantages in comparison to the other cell line models. For example, the genetic background of THP-1 cell line is homogenous leading to the minimization of the degree of variability in the phenotype of the cell. Another advantage is that the genetic modification of these cell lines by small interfering RNAs for the regulation of specific proteins is comparatively uncomplicated. The most regularly utilized read-out systems for reactions of THP-1 cells involves production of significant cytokines or transcription of the cytokines are significant and depends on the experimental designs, which are specific in nature (Chanput et al. 2015). 6. Methods of regulating chronic inflammation Chronic inflammation is usually results from the infection, which can be bacterial, viral, parasitic or fungal. Thus, the primary way to control chronic or persistent inflammation is to take precaution against infection by infection prevention methods. The primary prevention method is having a healthy diet by avoiding substances that induce inflammation. Therefore, getting control is very important (Kawasaki et al. 2012). Red meat should be avoided highly as it causes inflammation. Fries, which are rich in gluten, should be avoided as it causes chronic inflammation. Bad fat or Trans fat also have pro-inflammatory activities, refines carbohydrates, acid forming food can cause inflammation, which should be avoided. Today, most of the natural vegetables are grown by applying harmful pesticides, which are major causes of inflammation. Thus, vegetables should be washed before consumption very carefully. Candida is a major opportunistic pathogen, which causes inflammation through infection of gut. Thus, keeping a healthy gut is very important to control chronic inflammation (Chanput et al. 2015). 7. Bioactive Molecules Flavonoids and plant derived molecules Flavonoids encompass a group of phytochemicals, which have exhibited several effects of health and have been studied comprehensively (Vezza et al., 2016). They are secondary metabolites in plants and belong to the category of polyphenols. Among the six common classes of food flavonoids, the ubiquitous distribution of flavonols has been observed in different plant foods while noticeable quantities of isoflavones have been discovered in the foods that are obtained from leguminous plants (George et al. 2016). Flavonoids have exhibited promising health enhancing effects in human cell cultures, experimental human and animal clinical studies. They have exhibited hypocholesterolemic, anti-inflammatory and antioxidant effects together with the ability to adapt cell signaling as well as gene expression associated with the development of diseases (Haid et al. 2012). Sources and mode of action The sources of Flavonoids are fruits, vegetables and spices. They are rich in the fruits that grow on trees. Citrus fruits such as lemons, oranges and grapes contain a high amount of falavonoids (Paul Dzoyem et al. 2013). Beans such as kidney bean are high in flavonoids. Their best property is to protect the body against reactive oxygen species. They have discovered to possess antimicrobial, antiviral, anti-inflammatory and antihepatotoxic activities. They also possess biochemical effects that lead to the inhibition of a variety of enzymes such as phosphodiesterase, xanthine oxidase, aldol reductase, cycloxygenase and lipoxygenase. They also have a role in the regulation of a number of hormones such as androgens, thyroid hormone and estrogens. They also show anti-inflammatory activities in exudative as well as proliferative phases of inflammation (George et al. 2016). Anti-inflammation properties of flavonoids The anti-inflammation properties of flavonoids in cellular models engages the inhibition of the activities and synthesis of a number of pro-inflammatory mediators like adhesion molecules, cytokines, c-reactive protein and eicosanoids (Haid et al. 2012). The studies on humans which aims to investigate the effects of flavoniods on the inflammatory markers are inadequate and are primarily focused on the sources of food that are rich in flavonoids but not on the molecules that are pure. Several of the studies lack evaluation of absorption of flavonoids or fail to relate the effect off inflammation with an alteration in the circulating levels of flavonoids (Paul Dzoyem et al. 2013). Conclusion In this literature review, recent literatures have been reviewed regarding the chronic inflammation. Chronic inflammation is one of the basic steps that progress towards severe human diseases, while increasing the risk of fatal consequences including cardiovascular accident or cancer. In this literature review, the basic concept related to the chronic inflammation and how chronic inflammation is related to the severe diseases has been discussed. Recent research has been found direct relation between chronic inflammation prevention and consumption of dietary flavonoids. From different recent studies, it has been analyzed that flavonoids have anti-inflammatory activities, which could have major impact upon treatment and prevention of chronic inflammation. Thus, flavonoids can be used as prophylactic agents. The role of flavonoids has been discussed here. Further studies should focus on in-depth analysis of the natural product to establish its use in treating chronic inflammation relate d diseases. Reference List Aggarwal, B., Krishnan, S. and Guha, S., 2012.Inflammation, lifestyle, and chronic disease. Boca Raton: CRC Press. Chanput, W., Mes, J.J. and Wichers, H.J., 2014. THP-1 cell line: an in vitro cell model for immune modulation approach.International immunopharmacology,23(1), pp.37-45. Chanput, W., Peters, V. and Wichers, H., 2015. THP-1 and U937 Cells. InThe Impact of Food Bioactives on Health(pp. 147-159). Springer International Publishing. Cho, C. and Yu, J., 2012.From inflammation to cancer. Singapore: World Scientific. Daniluk, J., 2012.Meals that heal inflammation. Carlsbad, Calif.: Hay House. Dietert, R. and Luebke, R., 2012.Immunotoxicity, immune dysfunction, and chronic disease. New York: Humana Press. French, M., 2011.Inflammation in Chronic Disease Signature Initiative. Ottawa: Canadian Institutes of Health Research. Garca-Lafuente, A., Guillamn, E., Villares, A., Rostagno, M.A. and Martnez, J.A., 2009. Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease.Inflammation Research,58(9), pp.537-552. Gentile, L.F., Cuenca, A.G., Efron, P.A., Ang, D., McKinley, B.A., Moldawer, L.L. and Moore, F.A., 2012. Persistent inflammation and immunosuppression: a common syndrome and new horizon for surgical intensive care.The journal of trauma and acute care surgery,72(6), p.1491. George, V.C., Vijesh, V.V., Dehigaspege, A.I., Lakshmi, C.A., Anbarasu, K., Kumar, D.R., Ethiraj, R., Kumar, R.A. and Rupasinghe, H.P., 2016. Mechanism of Action of Flavonoids in Prevention of Inflammation-Associated Skin Cancer.Current medicinal chemistry. Guo, Y., Lip, G.Y. and Apostolakis, S., 2012. Inflammation in atrial fibrillation.Journal of the American College of Cardiology,60(22), pp.2263-2270. Haid, S., Novodomsk, A., Gentzsch, J., Grethe, C., Geuenich, S., Bankwitz, D., Chhatwal, P., Jannack, B., Hennebelle, T., Bailleul, F. and Keppler, O.T., 2012. A plant-derived flavonoid inhibits entry of all HCV genotypes into human hepatocytes.Gastroenterology,143(1), pp.213-222. Herder, V., Iskandar, C.D., Kegler, K., Hansmann, F., Elmarabet, S.A., Khan, M.A., Kalkuhl, A., Deschl, U., Baumgrtner, W., Ulrich, R. and Beineke, A., 2015. Dynamic changes of microglia/macrophage M1 and M2 polarization in theiler's murine encephalomyelitis.Brain Pathology,25(6), pp.712-723. Kawasaki, N., Asada, R., Saito, A., Kanemoto, S. and Imaizumi, K., 2012. Obesity-induced endoplasmic reticulum stress causes chronic inflammation in adipose tissue.Scientific reports,2. Lichti, P., 2012.Identification of metabolic markers for the development of chronic intestinal inflammation. Mathur, N. and Pedersen, B.K., 2009. Exercise as a mean to control low-grade systemic inflammation.Mediators of inflammation,2008. Paul Dzoyem, J., Hamamoto, H., Ngameni, B., Tchaleu Ngadjui, B. and Sekimizu, K., 2013. Antimicrobial action mechanism of flavonoids from Dorstenia species.Drug discoveries therapeutics,7(2), pp.66-72. Ashton Acton, P., 2012.Inflammation Mediators-Advances in Research and Application. ScholarlyEditions. Qin, Z., 2012. The use of THP-1 cells as a model for mimicking the function and regulation of monocytes and macrophages in the vasculature.Atherosclerosis,221(1), pp.2-11. Roy, S., Bagchi, D. and Raychaudhuri, S., 2012.Chronic inflammation. Boca Raton: Taylor Francis. Schillde, M., 2013.Structure function analysis of probiotic bacteria in mouse models of chronic intestinal inflammation. MuÃÅ'ˆnchen: Verl. Dr. Hut. Sica, A. and Mantovani, A., 2012. Macrophage plasticity and polarization: in vivo veritas.The Journal of clinical investigation,122(3), pp.787-795. Thilakarathna, S.H. and Rupasinghe, H.P., 2013. Flavonoid bioavailability and attempts for bioavailability enhancement.Nutrients,5(9), pp.3367-3387. Vezza, T., Rodrguez-Nogales, A., Algieri, F., Utrilla, M.P., Rodriguez-Cabezas, M.E. and Galvez, J., 2016. Flavonoids in Inflammatory Bowel Disease: A Review.Nutrients,8(4), p.211. Wick, G. and Grundtman, C., 2012.Inflammation and atherosclerosis. Wien: Springer-Verlag/Wien.