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University of Phoenix week 5 Budgetting Benefits Discussion

University of Phoenix week 5 Budgetting Benefits Discussion.

Part IWeek 5In light of the following comments, discuss the questions listed below:Budgeting time is an exciting time in every organization. Managers meet to come up with an estimate of needs for the areas and functions they supervise, and on the basis of the means available, new initiatives and projects are prioritized as to their perceived promise in adding to the growth of the organization.What is the relationship between strategic IS planning and the yearly budgeting and prioritization process? What is the objective of each? Do you think that general and functional managers should be involved in decisions about funding IS assets and services? Justify your opinion. Who should be developing and presenting the business case for a new IS? Why? How would the new and existing ISs be funded and who would fund them? Propose three funding methods, and discuss the advantages and disadvantages of each.Risks are associated with every new project that an organization considers to undertake. In the budgeting process, organizations often think of diversification of their new efforts and initiatives in order to minimize the risk of failure. What are the principal drivers and risks associated with implementing a new IS project? What are the principal drivers and risks associated with IS outsourcing? Why should an organization evaluate the aggregate risk of its portfolio of projects? What should an organization do if the current level of portfolio risk is not aligned with the degree of risk deemed appropriate according to the strategic IS plan? Justify your answers using relevant examples.PART IIThe Information Systems Security Impact PhaseThis week, you will evaluate the status of the security and its infrastructure for your case study from the perspective of professional and industry best practices, for example, CERT, SANS, (ISC)2, and existing national security and privacy acts, such as: the Health Insurance Portability and Accountability Act (HIPAA), the Computer Fraud and Abuse Act, the Electronic Communications Privacy Act (ECPA), the PATRIOT Act, the Gramm-Leach-Bliley Act (GLBA), the Sarbanes-Oxley Act (SOX), the Payment Card Industry Data Security Standard (PCI-DSS), or the Family Educational Rights and Privacy Act (FERPA). Depending on your case study some of the above regulations may or may not directly apply.Research security and privacy acts that are pertinent to your case study in the South University Online Library and on the Internet by using the following keywords:Health Insurance Portability and Accountability ActComputer Fraud and Abuse ActElectronic Communications Privacy ActUSA PATRIOT ActUSA PATRIOT Improvement and Reauthorization Act of 2005Public Law 107-56Gramm-Leach-Bliley ActSarbanes-Oxley ActPayment Card Industry Data Security StandardFamily Educational Rights and Privacy Act (FERPA)On the basis of your research, discuss the impacts of your case study analysis from the previous weeks on the security and privacy acts such as the ones listed above.Your report should include:A suggested plan for improving your organization’s operations securityThe information systems security impact of the constructed ISOn the basis of the system that you’ve developed so far, devise an annual budget to operate the following:Points of entry into the system where customers, or generally end users, are identified, authenticated, and authorized to access resourcesPoints of entry for assets (material or digital) obtained from suppliersSupport systems that track events, based on the system you’ve proposedSupport systems that track the traffic of information, based on the system you’ve proposedState the assumptions made on the operations of these systems. These assumptions may include the number of staff required, the pay rate, and the number of hours the different elements of the system operate per day.Your report should be written using the APA format, and it should include a copy of all the references used. Be sure your report contains the following:A logical flow and transition in the content.Complete report should include a title, abstract, summary, reference, and bibliography.Report should be an appropriate deliverable to senior management.Report should reflect depth, breadth, and implications related to the theories and constructs studied in this course.Conclusions and recommendations practical and actionable, not merely theoretical with no basis for the organization officers to take specific actions or steps to improve.Submission Details:Submit your plan in a 10–15 page Microsoft Word document, using APA style.
University of Phoenix week 5 Budgetting Benefits Discussion

Effect of the Financial Crisis on Canada

Effect of the Financial Crisis on Canada. Stability of Canadian Banking Sector in the Face of the Global Financial Crisis In September 2008 what started out as a housing bubble transformed into the worst recession that the United States had seen in decades. Although the crisis started in the developed countries, primarily the US and European countries, all countries around the world suffered from its adverse effects featuring bank failures and government bailouts. Canada, although close trading partners with the US, and Europe was the only G7 country (Refer to Fig. 1) with no bank failures or bailouts and faced a significantly milder recession (Haltom, 2013). Naturally, economists became interested in the cause for this stability, notable factors being Canada’s undeniable conservative approach and exceptionally strict regulation. Why were Canada’s banks stable in the face of the 2008 global financial crisis? This paper argues that the initial banking framework constructed in the early 19th century caused Canada’s banks to be stable. First, the resulting oligopoly allowed for easier regulation and implementation of restrictions by one overarching regulator. Second, Canadian banks, known to be less risky because of diversification allowed them to be less vulnerable to shocks. Lastly, with only 6 main competitors, there was low competition not leaving room for the shadow banking industry to thrive. This paper is organized as follows: by comparing Canada’s banking system with that of the USA we begin by highlighting the direction that the Canadian banking system took in the 19th and early 20th centuries. We then consider reasons why Canada demonstrated such resilience in the 2007-2008 financial crisis. Discussing this question will allow for other countries to learn and possibly implement the successful aspects of the Canadian financial system to better handle crises of this sort in the future. Figure Source: World Bank, 2012 Figure 1 GDP growth (%) and soundness of banking systems according to GCR (scale 1-7, 1=need bailouts, 7=sound) in G7 countries, 2008-09 Note that although, there exist trade-offs between stability and competition, defined as the “regulator’s dilemma,” the costs of stability won’t be identified nor will they be weighed against the benefits. This paper will focus primarily on the reasons that Canada remained stable in the face of the economic crisis in 2008. The stability of the Canadian banking system in the 2008 global financial crisis is not a singular event. Throughout history, the banking system in the US faced at least eight major banking crises in the antebellum era, under the National Banking system and until the Federal Reserve System was established in 1913, unlike the Canadian banking system that experienced two minor incidences in the 1830s associated with problems in the US (Bordo et al., 2011). This difference originated because of the establishment appointed the jurisdiction over chartering and regulating banks. In Canada, the federal government and in the US, the state government. A dual banking system emerged during the civil war when the national banking system was established in addition to the state banking system already in place. The American banking system restricted nation-wide branch banking whereas the federal jurisdiction in Canada allowed branching across provincial and territorial borders. In the British North American Act that combined four colonies to create Canada in 1867, the federal government was given absolute authority to build the banking framework. The Canadian banking system evolved into an oligopoly that Bordo, Redish and Rockoff described as “a cartel backed by the federal government and policed by the Canadian Bankers Association” as the need for a charter limited entry into the industry. Due to these initial institutional foundations, although Canada currently has 80 banks, 93 percent of the market share is dominated by only six with one financial regulator[1], Office of the Superintendent of Financial Institutions (OSFI) unlike the US that have managed to charter 7000 banks and multiple financial regulators (the Fed, Federal Deposit Insurance Corporation, Office of the Comptroller of the Currency and state regulators) (Haltom, 2013). OSFI supervises every aspect of the financial institutions: mortgages, insurance, investments, etc. Although branching is no longer prohibited in the US, this one restriction created a fragile and fragmented “unit banking[2]” in America as opposed to the highly concentrated and stable banking system in Canada in the face of the 2008 global financial crisis[3]. It is well known that Canada enforces strict regulations and restrictions on their financial system. Capital requirements such as capital adequacy regulatory standards, permissible capital deductions and regulatory capital are amongst the most restrictive in the world (World Bank 2012). Canada has greater debt regulation such as restrictions on leveraging and reduced incognito leverage or off-balance sheet (OBS) items. In addition to strict regulations, every five years, Canada reviews charters and regulations to incorporate and adapt to innovation and unfamiliar risks that may be developing. What allows these regulations and changes in restrictions to be feasibly enforced and easily implemented is the highly concentrated structure of the banking system. This facilitated coordination is also beneficial during a time of financial crisis. When discussing the 2008 global financial crisis, it’s important to note the role in lack of regulation and restrictions in causing it. The problems started with sub-prime[4] housing loans, which by 2006 were approximately 15 percent of pending mortgages in the US (Edey, 2009). There was a lack of regulation in identifying risk associated with administrating credit to borrowers with unreliable credit history and legitimate proof of income and lack of restrictions regarding loan-to-valuation ratio. The crisis continued to develop as the securitization of these sub-prime loans through mortgage-backed securities (MBSs)[5] and collateralised debt obligations (CDOs)[6] which are asset backed securities. These securities generated high returns and incorrectly received good credit[7] ratings by rating agencies attracting investors (Edey, 2009). The inevitable rise in mortgage delinquencies, reaching 11 percent at its peak, on these sub-prime mortgages that followed eliminated the confidence in these investments as the housing bubble burst. The first impact on the global financial markets was apparent when French banks suspended funds they were investing in US MBSs. Other European banks and OBS agents linked to them had also invested to a great degree in these securities making them prone to heavy losses (Edey, 2009). In contrast, Canada’s mortgage financing regulations aren’t structured to allow for such careless lending. In Canada, banks keep mortgages rather than selling them to investors. Before the financial crisis, approximately 30 percent of Canada’s mortgages were securitized, much less than the US which stood at almost 70 percent (Halton, 2013). In addition, less than three percent were sub-prime mortgages, significantly reducing the risk that Canada was exposed to as tight regulation encouraged safe mortgages (Halton, 2013). Financial institutions are prohibited from giving loans without at least a five percent down payment. If the down payment is less than 20 percent, mortgages are required to have insurance. Strict restrictions for insurance are also in place as it is only approved if total household debt-to-income ratio is less than 40 percent. These restrictions kept mortgage default rates below the historical average of less than one percent in Canada (BLACK**). This highly concentrated banking system also provided incentive to banks to engage in less risky activities as a single failure would severely injure the financial system. Due to the small number of institutions in effect their engagement in less risky activities, OSFI successfully prevented the failures that sub-prime mortgages brought to the global market from entering Canada’s banks. Figure Source: World Bank, 2012 Figure 2 Bank nonperforming loans (as % of total loans) in Canada, Japan, UK, and the US, 2008-09 The unit banking system of the US resulted in small, fragile and undiversified banks. There was a chartered bank per city or region with no branches. Historically, these small banks held similar assets which were primarily local loans and mortgages. Leading up to the 2008 crisis, most banks were engaging in MBSs and CDOs investments attracted by the promise of high returns. According to the Bond Market Association of the $25.9 trillion bond market, mortgage debt contributed to $6.1 trillion (Lambert, 2006). Already less diversified than banks in Canada sub-prime lending added to this risk. Rating agencies gave CDOs high credit ratings on the basis that they were backed by mortgages that were regionally diversified. The CDOs were incorrectly rated as they consisted of primarily sub-prime mortgages, the regions in which these mortgages were issued made little or no difference to their risk. The banks in Canada with nation-wide branching originally started off with geographically diversified assets, customers and risk constructed to be less risky which allows them to absorb shocks. With a small number of chartered banks, individual banks grew to be very large and in 1987 after the Bank Act was revised to increase competition, Canadian banks absorbed securities brokerages making them bigger than ever. This resulted in diverse sectors, investments as well as loans credited to customers. Canadian banks were now engaged in wealth management, insurance, mortgages lending, and securities brokerage (Pruss, 2015). Although attractive to smaller banks, the trade-off between higher return and high risk wasn’t one that Canadian banks needed to weigh. Only three percent of Canadian mortgages were sub-prime which further supports my argument that Canadian banks maintained diverse assets despite the pull of high return that CDOs and MBSs offered. The effects of this diversification were demonstrated historically with the small number of recessions and bank failures that Canada has faced in comparison with the US and in their ability to absorb shock in the 2008 financial crisis. The shadow banking activities, approximately 95 percent of the American economy played a large role in the global financial crisis (Haltom, 2013). Due to the highly concentrated nature of the Canadian banking system that fostered low competition and enforced tight regulation, the risky shadow banking industry didn’t have the same demand or freedom to grow the way it did in the US. The financial sector in the US consisted of two parallel banking systems, one that was regulated by multiple parties and another that transformed from investment banks and other financial intermediaries into the shadow banking industry, a market for activities restricted in the first (Bordo et al., 2011). Naturally, high risk activities gravitated towards the shadow banking industry which had vague restrictions and were mostly outside the regulatory umbrella (Haltom, 2013). This lack of regulation was followed by a lack of understanding in the risks associated with the industry as confidence levels were almost equal to that of the regulated sector. Krugmen (2009) claims that the problems associated with the crisis are less from deregulated institutions instead involve risks associated with “institutions that were never regulated in the first place.” As the shadow banking industry grew, the US moved towards the same financially vulnerable position that they experienced before the Great Depression. In addition, the Bush administration used their power and relation to the Office of the Comptroller of the Currency to eliminate any attempt to regulate sub-prime housing loans (Krugman, 2009). In the decades leading up to the global financial crisis, the Canadian banking system diverged further from that of the US. Following the 1987 Bank Act revision, Canadian banks began engaging in securities brokerages, mortgages and other activities that in the US, unregulated institutions partake in. OSFI overtook the affairs of the Inspector General of Banks as well as the Superintendent of Insurance becoming the sole regulator of all federal financial institutions in Canada overseeing in addition to the bank, pension funds, insurance and trust companies. With increasing risk, Canada increased their regulation. Only approximately 40 percent of the Canadian economy includes shadow banking activities, a considerable fraction of which Canada’s banks have committed to. In addition, 60 percent of these are insured and have access to lender of last resort thus protected by the federal government. The competitive and unregulated environment that allowed the shadow banking industry to grow in the US didn’t exist in Canada. Countries around the world were left crippled in the face of the 2008 global financial crisis, the most notable being the US where the crisis originated and developed. Canada was one exception as its banking system remained stable with no bank failures or government bailouts. Throughout history, in comparison to the US, Canada has suffered through less recessions, less panics and less bank failures. In the 2008 global financial crisis, Canada’s resilience is to be noted as it was a result of the nature the original banking framework created in the 19th century. Canada’s highly concentrated banking system allowed for tight regulation, diversification and low competition in the industry resulting in a less risky sector equipped to absorb the disastrous crisis of 2008. Although, Canada’s history has played a large part in constructing this stable system and any one solution or explanation for financial stability won’t miraculously save a nation, there is a great deal that other countries can learn from Canada to better equip themselves to handle crises in the future. References Bordo, Michael D., Angela Redish, and Hugh Rockoff. “Why Didn’t Canada Have a Banking Crisis in 2008 (Or In 1930, Or 1907, Or…)?” National Bureau of Economic Research Working Paper No. 17312, August 2011. Haltom, Renee. “Why was Canada Exempt from the Financial Crisis?” Econ Focus, Fourth Quarter, 2013, pp. 22-25. Refer to: https://www.richmondfed.org/~/media/richmondfedorg/publications/research/econ_focus/2013/q4/pdf/feature2.pdf World Bank. Crisis-proofing financial integration: Canada, June 2012, pp. 30-33. Refer to: http://siteresources.worldbank.org/ECAEXT/Resources/258598-1284061150155/7383639-1323888814015/8319788-1324485944855/03_canada.pdf Edey, M. (2009), The Global Financial Crisis and Its Effects. Economic Papers: A journal of applied economics and policy, 28: pp. 186-195. Refer to: http://onlinelibrary.wiley.com/doi/10.1111/j.1759-3441.2009.00032.x/full Krugman, Paul. The Return of Depression Economics and the Crisis of 2008. New York: W.W. NortonEffect of the Financial Crisis on Canada

Japan Growth Figures Essay

write my term paper The article explores the poor growth figures of Japan as well as the dismal improvement in the Gross Domestic Product (GDP). According to Obe (2014), the economic downturn that was witnessed in 1997 was mainly fuelled by an increase in sales tax. Even though Mr. Abe’s government was fully conscious of the cause, austerity measures were not put in place. In order to cushion the current economic turmoil, over $50 billion stimulus package has been dispatched by the government. Frontloading of the expenditure phase is expected to kick off from the month of April to September 2014 (Obe, 2014). The export volume has dwindled over the past 12 months, largely due to the weak yen. This implies that exporters cannot significantly benefit from export trade due to the unfavorable foreign exchange rates. It is prudent to mention that Japan’s export engine heavily depends on the strength of the Yen. As it stands now, the nation’s consumers have found it quite cumbersome to bear the brunt of economic stagnated growth. The last quarter mark of 2013 gave a clear indication that the country’s economy was going to perform below the expectation due to the 1 % annualized growth rate (Obe, 2014). The article relates a number of economic concepts discussed in the course materials. First, the concept of the Gross Domestic Product (GDP) stands out as the main topic being addressed in the article. The author observes that the rise in sales tax has heavily contributed to the minimal improvement of Japan’s Gross Domestic Product (GDP). The term “growth rate” has also been used in the article to expound the slow pace at which Japan’s economy is expanding. For instance, the rise in sales tax from 5 percent to 8 percent in the current financial year is expected to trigger a further economic chill or sluggish growth rate. Although GDP growth did not drop in value, it experienced a marginal improvement over the last financial year. The author argues that the slight growth in the GDP index may have been contributed by the high demand for more costly products. GDP was also affected by a gross surge in imports. ‘Gains from trade’ is also another concept that can be derived from the article. As already mentioned, expensive goods brought a lot of gains to local traders. It is apparent that the quality of goods sold is a major consideration for local consumers in Japan. Get your 100% original paper on any topic done in as little as 3 hours Learn More Apart from the economic concepts learned in the course, there are other perspectives and deeper insights that can be identified from the news article. For example, a weak Japanese Yen has led to unfavorable foreign exchange (Forex), especially in the export market. Another typical economic term that can be identified in the article is household spending. The latter grew modestly by a margin of about 0.5 %. Although the impact of supply on GDP has not been discussed in the article, it is a crucial factor that may either hamper or boost the economic growth of any economy. For a country like Japan, export trade is the chief economic mainstay. However, the country did not supply adequate exports in foreign markets during the previous fiscal year. This led to reduced cash inflow from foreign exchange. The 0.7 percent drop in exports during the third quarter of 2013 was a major economic blow for Japan. Factors such as real wages, asset prices, consumer confidence, and interest rates should be used to compute the aggregate demand in order to obtain the actual Gross Domestic Product of an economy. Reference Obe, M. (2014). Japan growth figures disappoint; gross domestic product increase comes in well below expectations. Wall Street Journal (Online). Web.

Symptoms Of Gastrointestinal Inflammatory Diseases Health And Social Care Essay

Inflammation is a type of defence mechanism that the body exhibits in response to damage to part or all of its tissues. Depending on the severity of the insult and consequent damage to cells, the inflammatory response involves recruitment of varying proportions of neutrophils, eosinophils, basophils, lymphocytes (both T and B cells), natural killer cells and cells of the monocyte macrophage lineage. Inflammation normally seeks to eliminate the cause of the insult and repair the damage caused. However, if the damage persists, persistent recruitment of inflammatory cells to the injured area will lead to further damage leading to chronic inflammation. [9] The gastrointestinal (GI) tract is a hollow muscular tube running from the mouth to the anus. It is about 7 to 9 meters long in adult. The enormous mucosal surface, which is the innermost layer of the gastrointestinal tract, is constantly exposed to a plethora of antigenic, mitogenic, mutagenic, and toxic stimuli thus clearly making the gastrointestinal tract vulnerable to such inflammatory responses. [10] Gastrointestinal inflammatory diseases Inflammation can affect any part of the gastrointestinal tract. Inflammatory Bowel Disease The inflammatory bowel diseases (IBD) are chronic inflammatory diseases affecting the gastrointestinal tract. IBD encompasses two forms of intestinal inflammation, namely ulcerative colitis and Crohn’s disease. Crohn’s Disease may affect all parts of the gastrointestinal tract, but more commonly it involves the distal part of the small intestine and the colon. On the other hand, ulcerative colitis results in colonic inflammation which can affect only the rectum, or can progress proximally to involve the colon, either partly or entirely [11]. Currently, the etiology of IBD is unknown, but recent investigations have identified contribution of genetic, environmental as well as immunological factors underlying the disease [12]. Susceptibility to disease is thereby determined by genes encoding immune responses which are triggered by environmental stimuli [13]. Figure 1.1 shows a combination of genetic and environmental culprits triggering activation of intestinal immune and non-immune systems which culminate in inflammation and tissue damage. [14] Figure 1.1: Etiology and pathogenesis of IBD. Current medical therapy of IBD consists of salicylates, corticosteroids, immunosuppressants and immunomodulators. However, their use is associated with severe side effects and complications, such as an increased rate of malignancies or infectious diseases. [15] Gastritis (Inflammation of stomach lining) Gastritis represents a group of disorders characterized by gastric epithelial cell injury and regeneration together with the induction of inflammatory changes in the gastric mucosa [16]. Inflammation of the gastric mucosa occurs as a result of an imbalance between mucosal defensive and aggressive factors. It is now well – established that H. pylori infection is the cause of the most common form of chronic gastritis [17]. Studies have established that H.pylori directly contributes to abundant inflammatory response and cause injury to gastric epithelial cells through elaboration of cytotoxic factors and it may also make gastric epithelial cells more susceptible to carcinogenic conversion [18]. There is also evidence that drugs and alcohol may cause gastritis. Iron therapy has also been implicated as a cause of gastritis. Iron-pill gastritis involves mucosal erosion which is accompanied by acute and chronic inflammation and marked regenerative epithelial changes [19]. Autoimmune and hypersensitivity reactions may also be culprits in gastritis. [20] Esophagitis (Inflammation of the oesophagus) Eosinophilic esophagitis is a chronic inflammatory condition whereby presence of dense eosinophilic inflammation of esophageal mucosa contributes to esophageal dysfunction. Eosinophilic esophagitis is a newly acknowledged disease whose incidence and prevalence is rapidly increasing in developed and developing countries [21]. The disease is a major cause of gastrointestinal morbidity among children and adults. It is thought to be immune mediated, whereby food or environmental antigens trigger a T-helper (Th)-2 inflammatory response. [22] Pancreatitis Chronic pancreatitis is well-known as a persistent inflammatory disorder of the pancreas, characterized by destruction of the pancreatic parenchyma, maldigestion, chronic pain and diabetes mellitus. Susceptibility to chronic pancreatitis is inherited in a complex manner, involving mutations in several genes conferring various degrees of risk. [23] Although the exact etiology of acute and chronic pancreatitis is unknown, studies have revealed that they are most frequently caused by a high consumption of alcohol and tobacco [24]. Other common causes include gallstones, hypertriglyceridemia, hyperparathyroidism, trauma, pancreatic tumors, and intra-abdominal and non-abdominal surgery. Drugs constitute a relatively infrequent cause of acute pancreatitis and account for 1.4 to 2% of the cases in the general population. [25] Gastroenteritis Gastroenteritis refers to inflammation of the gastrointestinal tract, involving the stomach and intestines. Acute gastroenteritis is a common disease occurring worldwide, which affects all age groups and leading to an estimated three million deaths annually. In many patients the causal agent cannot be identified, but research has implicated bacteria and parasites as well as viruses such as rotavirus, adenovirus, and caliciviruses as major culprits in causing gastroenteritis. [26] Symptoms of gastrointestinal inflammatory diseases Table 1.1: Symptoms of GI inflammation Gastrointestinal Inflammatory Disease Symptoms Inflammatory Bowel Diseases Diarrhoea Blood in stools Gastrointestinal bleeding Abdominal pain Fistulas (usually around the rectal area, may cause draining of pus, mucus, or stools) Constipation Weight loss [11] Gastritis Nausea Vomiting (possibly with blood) Abdominal pain and bloating Indigestion Loss of appetite Blood in the stools. [27] Esophagitis Food impactions Dysphagia (difficulty swallowing) Nausea Vomiting Heartburn chest pain or abdominal pain [28] Pancreatitis Abdominal pain Nausea Vomiting Weight loss Mild yellowing of skin (jaundice) Fatty stools [29] Gastroenteritis Abdominal pain Nausea and vomiting Diarrhoea Joint stiffness or muscle pain Poor feeding and weight loss [30] Biomarkers of Gastrointestinal inflammation Inflammatory activities occurring within the gastrointestinal tract can be assessed using a variety of techniques. Presently, the most reliable means to assess intestinal inflammation is endoscopy with mucosal biopsy. However, this technique is expensive, invasive, time-consuming and is not popular with patients [31]. Moreover, this technique requires a skilled operator and an uncomfortable preparatory regimen. Other techniques constitute measurement of conventional non-invasive acute-phase inflammatory markers in plasma and faeces. [32] Blood inflammatory biomarkers Serological biomarkers are principally produced when the intestine is exposed to the normal commensal bacteria and their increased levels might be indicative of an impaired or wrongly regulated inflammatory response. Erythrocyte sedimentation rate (ESR), white blood cell count (WBC) and C-reactive protein (CRP) are well-established indicators of inflammatory conditions within the intestine. [33] C-reactive protein (CRP) CRP is one of the vital acute phase proteins in humans, which is normally produced in low quantities by hepatocytes (<1 mg/L). However, in the event of an acute phase stimulus like inflammation, hepatocytes amplify production of CRP and may reach peak concentrations of 350-400 mg/L. In vivo, CRP is involved in opsonisation of infectious agents and damaged cells. [34] C- Reactive protein is an objective marker of inflammation and, in gastrointestinal diseases such as Crohn’s disease and acute pancreatitis, its levels correlate well with clinical disease activity. [35] Table 1.2: Advantages and disadvantages of C-Reactive Protein Inflammatory Biomarker C-reactive protein Advantages Rapid response to inflammatory stimulus Unaffected by age and gender Quantitation is precise and reproducible [36] CRP has a short half life (19 hours) in comparison with other acute phase proteins and its level will increase early after the onset of the inflammation and also rapidly decline after inflammation has been resolved. [34] Disadvantages Less clinical information available. Relatively more expensive than ESR. [36] Erythrocyte sedimentation rate (ESR) ESR refers to the rate at which erythrocytes migrate through the plasma. [34] Table 1.3: Advantages and disadvantages of erythrocyte sedimentation rate Inflammatory Biomarker Erythrocyte sedimentation rate Advantages Inexpensive Much clinical information available [36] Disadvantages Affected by age, gender and red blood cell morphology [36] ESR is affected by conditions such as anaemia, polycytemia, as well as thalassemia. [34] Reflects levels of many plasma proteins [36] Responds slowly to inflammatory stimulus. [36] In comparison with CRP, ESR levels peak much slowly, and may also take many days to decline, even if the inflammatory condition has subsided. [34] Faecal biomarkers in gastrointestinal inflammation Increased translocation of granulocytes into the intestinal mucosa during inflammatory conditions results in excretion of elevated amounts of proteins from these cells in faeces. Inflammatory mediators detectable in faeces have been recognised as candidate biomarkers in intestinal inflammation as they are non-invasive, simple, sensitive and specific parameters useful to assess gastrointestinal inflammation. [32] Indium-111-labeled leucocytes Detection of Indium-111-labeled leucocytes in faeces is regarded as the gold standard stool marker of gastrointestinal inflammation. [37] Table 1.4: Advantages and disadvantages of Indium-111-labeled leucocytes Faecal Biomarker 111indium labelled neutrophils Advantages Specific, quantitative, and sensitive measure of intestinal inflammation. [38] Disadvantages It requires special sterile labelling facilities. It is costly, in terms of patient’s hospitalization, analysis and disposal of isotopic material. (about £300/patient) It involves exposing patients to ionizing radiation. There are practical problems with obtaining complete faecal collections over four days. [38] The complexity of this technique, as well as its high cost and the exposure of patients to ionizing irradiation have limited its use thus prompting research to be oriented towards more simple and cost-effective alternatives to the indium-111 technique. In this regard, faecal calprotectin has been proposed as an excellent candidate. [39] Calprotectin Calprotectin was first described by Magne Fagerhol and collaborators in 1980. Calprotectin is a small calcium- and zinc-binding protein which originates from neutrophil granulocytes. It is estimated that the amount of calprotectin in each granulocyte is equivalent to the amount of haemoglobin in an erythrocyte (about 20 pg of calprotectin per granulocyte). Besides having an antimicrobial function, calprotectin plays a role in inhibition of several metalloproteinases and induction of apoptosis in both malignant and non-malignant cell cultures. It is also assumed that calprotectin plays a key role in regulating the intestinal microbiota. Since the intestinal mucosa is under constant exposure to a plethora of microbes and their harmful products the concentration of calprotectin is much higher in normal intestinal environments as compared to the amount of calprotectin in blood. In inflammatory conditions the concentration of calprotectin may rise to over 100 folds of its normal value [40]. Detection of calprotectin in tissue samples, body fluids, and stools therefore provides a non-invasive means to assess the presence of intestinal inflammation. Health conditions which lead to abnormally elevated calprotectin levels include active rheumatoid arthritis, meningococcal sepsis and active inflammatory intestinal disease [41] as well as in other organic gastrointestinal diseases such as diverticular disease, infectious enterocolitis, nonsteroidal anti-inflammatory drug (NSAID) enteropathy, and cancer. [42] Table 1.5: Advantages and disadvantages of Calprotectin Faecal Biomarker Calprotectin Advantages Faecal calprotectin has several characteristics of an ideal test: simple, non-invasive, reproducible and relatively low cost. It is stable for 3 to 7 days at room temperature and when the faeces are at -20°C no change in calprotectin has been observed over time. It resists enzymatic degradation both in vivo and in vitro, thus calprotectin levels can be measured in the stools easily. Calprotectin is unaffected by medication and dietary supplements. It can be conveniently assessed in small samples. [43] Calprotectin is not a disease specific marker and thus easily detects inflammation throughout the whole gastrointestinal tract. Studies have reported increased levels of faecal calprotectin in IBD patients as well as in those with several other inflammatory conditions of the lower gastrointestinal tract. [44] Calprotectin significantly correlated with four day faecal excretion of 111indium which is the gold standard stool biomarker of intestinal inflammation. [45] Disadvantages Use or nonsteroidal antiinflammatory drugs (NSAIDs) can lead to elevations in calprotectin levels. Hence, NSAIDs treatment should be stopped before taking faecal samples for calprotectin determination. The most evident criticism of the faecal tests is that they are not acceptable to patients and they are generally unpleasant to work with. [46] Menstrual bleeding or other bleeding in the body above 100 ml might lead to elevated faecal calprotectin levels. Faecal calprotectin is generally assumed to be evenly distributed; however some authors suggest that there may be significant intra-individual biological variations in calprotectin levels caused by other factors excluding disease. Faecal calprotectin levels are raised in any condition that leads to neutrophil translocation to the gut, such as in infections and neoplasms. Thus, the sensitivity of faecal calprotectin is not as high as desired. [33] Lactoferrin: Lactoferrin is an iron-containing glycoprotein secreted by the majority of mucosal membranes. It is the main component of secondary polymorphonuclear granules, which are the prime cells of an acute inflammatory response. In intestinal inflammation, leukocytes invade the mucosa, which results in an increase in the excretion of lactoferrin into the faeces. [47] Besides calprotectin, faecal lactoferrin is apparently the most widely employed as a biomarker of intestinal inflammation. [46] Table 1.6: Advantages and disadvantages of lactoferrin Faecal Biomarker Lactoferrin Advantages It can be detected using simple and relatively cheap techniques. The quantification of lactoferrin concentration in faeces is done using the relatively inexpensive and easy enzyme-linked immunosorbent assay (ELISA) technique. It has excellent stability in faeces over a long period of time. [46] Studies have shown that faecal lactoferrin is a highly sensitive and specific marker for detecting intestinal inflammation. [47] It is a measure of mucosal inflammation which is detectable at a concentration which is inadequate to bring about an increase in levels of ESR and CRP. [46] A study revealed that lactoferrin was the better neutrophil-derived faecal biomarker of inflammation as compared with elastase, lysozyme and myeloperoxidase, in terms of its better accuracy and cost-effectiveness. [37] Faecal lactoferrin is highly precise in distinguishing organic from functional intestinal diseases. [37] Disadvantages Some studies have suggested that lactoferrin is less accurate of lactoferrin than calprotectin for detection of intestinal inflammation. [37] NSAIDs intake may increase lactoferrin levels, perhaps owing to the associated induced enteropathy. Faecal tests are frequently criticised in that they are generally not acceptable to patients and nasty to work with. [46] Factors affecting gastrointestinal inflammation Drug use and gastrointestinal inflammation A number of the frequently used drugs today may have deleterious effects on the gastrointestinal system and have been associated with gastrointestinal inflammatory diseases. Drugs causing Colitis The frequency of colitis which is induced by drugs is often under estimated. Studies have found that colitis may be induced due to antibiotics, NSAIDs, laxatives, vasoconstrictive agents, oestroprogestatives [48]. Pseudomembranous colitis is caused by antibiotics which facilitate an overgrowth of Clostridium difficile. Hemorrhagic colitis can be induced by antibiotics such as penicillin, amoxycillin and ampicillin. Ischemic colitis may be caused by drugs which induce mesenteric vasoconstriction [49]. More recently, cases of colitis caused by non-steroidal anti-inflammatory drugs (NSAIDs) are increasingly being reported. However, the mechanism of NSAIDs-induced colitis is still not known. [50] Toxicity of NSAIDs to mucosal cells might cause increased intestinal permeability, which is a prerequisite for colitis. [51] Drugs causing Inflammatory bowel diseases (IBD) A number of drugs have been incriminated as causing or aggravating IBD. These include antibiotics, NSAIDs and oral contraceptives. [52] Classes of drugs responsible for GI inflammation NSAIDs: Non-steroidal anti-inflammatory drugs (NSAIDs) are some of the mostly used pharmaceuticals worldwide, and are particularly useful in prevention and treatment of pain and inflammatory diseases. Prostaglandins, produced by arachidonic acid metabolism via the cyclooxygenase enzymes are largely involved in conferring protection to gastric mucosa. NSAIDs inhibit the production of both cyclooxygenase enzymes (COX-1 and COX-2), and thereby decrease the production of prostaglandins that leads to the antiinflammatory, antipyretic, and analgesic effects of NSAIDs. However, inhibition of prostaglandin production may be related to an increase in the formation of leukotrienes which attract inflammatory cells, causing local sites of inflammation. [53] The main pathogenic effect of NSAIDs on intestinal mucosa is the increase of mucosal permeability that results in subsequent development of small intestine inflammation. [54] Nearly three-quarters of patients on long-term treatment with NSAIDs have small-intestinal inflammation [55]. The small intestinal inflammation which is induced by NSAIDs has been associated with blood loss and protein loss [56]. NSAIDs intake has been associated with several gastrointestinal inflammatory diseases. Studies have suggested association of the use of indomethacin, piroxicam, ketoprofen, naproxen, rofecoxib and celecoxib with acute pancreatitis [57]. In addition, some authors have put forward NSAIDs as a cause of diffuse chemical or reactive gastritis; however this has not been explicitly documented in studies involving pre- and post-treatment biopsies [58]. Studies have also shown association between NSAID intake and appendicitis in the elderly [59]. Studies have shown that over the long run, NSAIDs treatment leads to small bowel inflammation as depicted by increased translocation of indium 111-labeled leucocytes into the ileum. Recent studies have also associated mucosal inflammation with NSAIDs treatment as revealed by increased faecal calprotectin shedding. The severity of calprotectin shedding and leukocyte migration was however independent of the type or dose of NSAID taken. [56] Oral contraceptives: One of the adverse effects of oral contraceptives is that estrogens can lead to increased blood levels of triglyceride and hypertriglyceridemia is one of the well-established causes of pancreatitis. Thus common estrogen-containing treatments and conditions including birth control pills, hormone replacement therapy for menopause, tamoxifen treatment, clomiphene treatment for polycystic ovary syndrome and pregnancy may play a role in etiology of pancreatitis. [60] Studies have supported that estrogens are an uncommon but well-known risk factor of pancreatitis in women and men with pre-existing hyperlipidemia. [61] Oral contraceptive use also was associated with risk of Crohn’s Disease and ulcerative colitis. [62] Statins: Statins, also known as the 3-hydroxy-3-methylglutaryl-coenzyme (HMG-CoA) reductase inhibitors, are the most frequently prescribed lipid-lowering agents existing on the market. Several observational studies have associated statin therapy with pancreatitis [63]. While the use of statin therapy was associated with reduced risk of pancreatitis in patients with normal or mildly elevated triglyceride levels [64], on the other hand statin therapy has surprisingly also been implicated in the etiology of pancreatitis. However, the exact mechanism by which statins cause pancreatitis is not known [65]. Acute pancreatitis has been reported from some cases undergoing treatment with atorvastatin, fluvastatin, lovastatin and simvastatin [66]. According to studies, though statin-induced pancreatitis can occur at any time, its incidence seems very uncommon early on and is more likely to arise after several months of therapy. [67] Antihypertensive medications: Angiotensin-converting enzyme (ACE) inhibitors widely prescribed for treatment of hypertension are usually well-tolerated; however acute pancreatitis has been reported in a few cases treated with lisinopril, captopril, and enalapril [68]. Case studies have also pointed towards Enalapril maleate as inducing eosinophilic gastroenteritis [69]. Loop diuretics and hydrochlorothiazides have also been incriminated in drug-induced acute pancreatitis. [70] Antibiotics and Antimicrobials: Tetracycline class of antibiotics has long been implicated as an etiologic factor in acute pancreatitis [71]. A similar association with acute pancreatitis has also been demonstrated with sulphonamides. [72] Corticosteroids: Chronic treatment with corticosteroids apparently heightens the risk of developing adverse gastrointestinal events including ulcers and bleeding in patients. The results of a recent study suggested slight risk of adverse gastrointestinal events, mainly gastritis, in patients who were prescribed inhaled corticosteroids, whereby significant amount of inhaled corticosteroid appeared in the gastrointestinal tract, notably in the lining of the oesophagus, the stomach, intestine, and the colon. [73] Proton pump inhibitors: These are highly potent gastric acid-suppressants in clinical use [74]. Intake of proton pump inhibitors has recently been associated with increased faecal calprotectin. [75] Central Obesity and Gastrointestinal inflammation Obesity, defined as the excessive accumulation of body fat, affects a massive proportion of the world’s population. However, measurement of body fat is a challenging task. Virtually, all social science research on obesity make reference to the person’s body mass index (BMI) which is a simple, rapid, and inexpensive method. According to this method, normal range is 19-24.9 kg/m2, overweight is 25-29.9 kg/m2, and obesity >/= 30 kg/m2. However, this method has been subjected to criticism because it does not distinguish fat from fat-free mass such as muscle and bone [76]. In addition, it has also been observed that for the same value of BMI, women are, on average, fatter than men, and Asians are, on average, fatter than Caucasians [77]. Distribution of body fat is highly important in evaluating obesity-related health risks. It has been well-established that accumulation of intra-abdominal fat, that is central obesity, shows stronger correlation with disease states in comparison with total body fat [78]. According to a recent study, waist circumference, and not BMI, explains obesity-related health risk. [79] Obesity is associated with low-grade inflammation. The inflammatory process originates and resides mainly in adipose tissue, as it is responsible for production and secretion of various proteins involved in development of obesity related adverse health effects [80] . Through this mechanism, increasing obesity leads to reduction of adiponectin levels, which has anti-inflammatory properties, and to elevated levels of C-reactive protein (CRP) and results in systemic inflammation, including gastrointestinal inflammations. Intestinal inflammation is a key feature in severe obesity [81]. A study has established diet-induced intestinal inflammation as an early biomarker and mediator of obesity [82]. Findings in adult humans and in animals have suggested that the inflammatory status at mucosal surfaces of various organs including the adipose tissue, ooesophagus, pancreas, colon, which are associated with the increase of fat mass, may be involved in the pathogenetic pathways of obesity complications [81]. In addition, animal studies showed that obese mice display enhanced intestinal permeability [83]. Recent epidemiological studies have demonstrated that obesity is associated functional bowel disorders, which may have resulted from a low-grade inflammation [81]. Furthermore, obesity has been found to increase the severity of acute pancreatitis through amplification of the immune response to injury [84]. Obesity, especially abdominal obesity, was also found to be a significant risk factor for erosive esophagitis [85]. Very recently, an association of obesity with endoscopic gastritis was demonstrated. [86] Results of a recent study pointed that circulating neutrophils are greatly activated in severely obese subjects, thereby indicating the association between obesity and activation of the innate immune response. In addition, elevated levels of faecal calprotectin, which is a non-invasive biomarker of intestinal inflammation, have been reported in individuals with high BMI [87]. Another study demonstrated a strong correlation between circulating calprotectin levels with abdominal adiposity in Japanese men, and also showed that weight loss in the subjects led to decreased circulating calprotectin. [88] Genetics Gastrointestinal inflammatory diseases may also be influenced by genetic components. Family studies have revealed strong familial association and high sibling risk ratio in etiology of eosinophilic esophagitis. [89] Genetic factors also play a role in pancreatitis. [90] In addition, increased familial risk has also revealed a genetic basis in Inflammatory Bowel Disease [91], and an increased faecal calprotectin concentration has also been demonstrated in asymptomatic first-degree relatives of IBD patients, thus indicating a high prevalence of subclinical intestinal inflammation in them. [92] Gender Gender may play a role in gastrointestinal inflammatory diseases. Animal studies in mice have demonstrated that females develop more severe intestinal inflammation than do males [93]. On the other hand, a study has shown that bile reflux gastritis was more frequent to male gender [94]. Another study found a positive correlation between the male sex and pancreatitis [95]. Additional studies found that there is a slight preponderance of colitis ulcerosa in men and of Crohn’s disease in women [96]. Lifestyle factors Smoking Cigarette smoking affects ulcerative colitis (UC) and Crohn’s disease (CD) in very different ways. According to recent studies, smoking cigarettes has a negative effect on the course of CD, and that smoking cigarettes may have a protective effect in some patients with UC [97]. Conversely, smoking cessation aggravates ulcerative colitis and improves CD [98]. Furthermore, studies showed that smoking conferred a strong, independent and dose-dependent risk of pancreatitis that may be additive or multiplicative when combined with alcohol. [99]. Alcohol Most cases of chronic pancreatitis are alcohol-related. [100] However, a recent study showed that faecal calprotectin concentrations in active-drinking alcoholics were not significantly different from the healthy controls thereby indicating the absence of a subclinical intestinal inflammation involving activation of neutrophils in the alcoholics. [101] Diet Pro- or prebiotics will directly influence the microbial flora, while immunonutrition, including omega-3 fatty acids and certain polyphenols, including green tea polyphenols, may reduce the symptoms of gut inflammation [102]. Studies have shown that lycopene, an antioxidant which is abundantly found in foods that have a natural red color such as tomato and watermelon, may play a role in attenuating the inflammatory process [103]. A study showed that intestinal bacteria and high fat diet interact to promote proinflammatory changes in the small intestine [104]. Certain studies suggested that refined sugar consumption might be a risk factor for Crohn’s Disease, but not Ulcerative Colitis. Fat intake is reportedly positively associated with ulcerative colitis [105], whereas vegetables and fiber consumption seem to decrease GI inflammatory process as shown by decreased faecal calprotectin [106]. Stress Psychological stress reportedly increases disease activity in inflammatory bowel disease by both direct and indirect mechanisms as shown below. [107] Figure 1.2: Direct and indirect ways by which stress can aggravate Inflammatory Bowel Diseases Socioeconomic status Epidemiological studies have demonstrated Inflammatory Bowel Diseases to be more prevalent among people of high socioeconomic status. Such an occurrence was explained by the ‘hyegiene hypothesis’, according to which individuals with higher standards of living may be living in cleaner environments and thus are more protected from childhood infections, but however exposure to infectious agents later in life makes them more vulnerable to chronic intestinal inflammation in adulthood [108]. A study in China demonstrated that levels of faecal calprotectin were significantly increased in the rural infants as compared to urban ones. [5] Gastric surgery Partial gastrectomy increases the risk for chronic pancreatitis in male alcoholics [109]. Appendectomy has possibly protective effects in ulcerative colitis but it is suggested as a risk factor in Crohn’s disease. Tonsillectomy is a risk factor for developing Crohn’s disease. [110]

Article Analysis Presentation

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Article Analysis Presentation

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