Business Analysis Business Analytics Essay - 1990 Words

Business Analytics is focused on the latest business intelligence tools, technology and trends for business executives who plan, build, and use business intelligence products and solutions. Today great business intelligence and analytic technologies are allowing big companies to go big, go fast, go deep, go cheap and go mobile with business data. Business Analytics is used to analyze large amounts of data by applying statistical tools and techniques in order to generate business insights. The key to this ability is this company’s closed loop of testing, learning, and acting on new opportunities. In this company, Analytics has become such a focus that all analytical people were recently combined into one organizational unit. Thus the extensive use of analytical and business performance has transformed their ability to compete on analytics into a key point of differentiation and lasting competitive advantage. This company had to come up with viability of potential customers in the market, product research, and marketing campaigns and lead generation. All the activities expected of Siemens Healthcare company were attained through the help of analytics. Analysis I had interned in other companies in the past, but none the companies had an elaborate analytical driven marketing campaigns that were result oriented. The very concept of market analytics was new to me. The process enabled the project managers to evaluate the success of the marketing implementation through theShow MoreRelatedBusiness Analysis : Business Analytics Essay944 Words   |  4 PagesBusiness Analytics Business Analytics, is a system that use various techniques and processes to gather information to used be used to make business decisions. The data is used to answer a question. Often this is used in marketing. It helps to take away some of the â€Å"guess work† out of who market will target. 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Human Resource Management & Leadership-Free-Samples for Students

Questions: 1 Describe how this Initiative would Impact the Induction Program for new frontline Managers joining Ambulance Service NSW. 2 The focus of this Program has been on Managers. What learning and development now needs to be undertaken for the following positions to further support the change in focus for the Organisation? Answers: 1.This initiative would impact the induction program for the new frontline manages. The new things to be incorporated are: The frontline managers should be engaged early in the learning culture Personal analysis- In order to determine the importance of the Ambulance Management Qualification and its relevance it is required to undertake a personal analysis Evaluation- to determine the effectiveness, the frontline managers must be tested before and after the initiative being taken Performance analysis-the results of performance after the initiative should be analysed to identify the areas of improvement. It may include modifying the 12 day programme (O'Meara 2015) 2.Learning and development needs that are to be undertaken for- Frontline operational staff and Customer service staff- microanalysis and personal analysis of these staff is required because they do not participate in AMQ. Instead, they also manage staff Moreover, the macro analysis of the organisation has already been conducted but the task analysis was not conducted. Further, based on this analysis, there is need of development of tailored LD. It may include online learning to increase opportunities, leadership training, executive development and cross cultural training (Francis and Mazany 2013). References Francis, S.D. and Mazany, P.C., 2013. Developing elements of a learning organization in a metropolitan ambulance service: strategy, team development and continuous improvement.Health manpower management. O'Meara, P., 2015. Searching for paramedic academics: vital for our future, but nowhere to be seen!.Australasian Journal of Paramedicine,4(4).

Clinicopathological Correlates of Adrenal †Free Samples to Students

Question: Discuss about the Clinicopathological Correlates of Adrenal. Answer: Introduction: Elevated levels of cortisol hormone are mainly responsible for the occurrence of Cushing syndrome. Cortisol is mainly produced by adrenal glands in the body. Cortisol performs important functions in the body like regulation of blood pressure and normal functioning of cardiovascular system. Cortisol is also helpful in responding to stress and metabolizing carbohydrates, proteins and fats in the usable energy. However, elevated levels of cortisol, disrupt these physiological processes and lead to development of Cushing syndrome. Cortisol levels in MV might increase due to high levels of stress, malnutrition, depression and high levels of emotional stress. Cortisol levels in a person can also increase due to athletic training, alcoholism and panic disorders. High doses of anti-inflammatory medications like corticosteroids might increase cortisol levels. Pituitary gland releases more adrenocorticotropic (ACTH) hormone in pituitary gland tumor. This increase in the adrenocorticotroic horm one is known as Cushings disease. Adrenal gland abnormality or tumor might cuase Cushings syndrome. Even though70 80 % cases of the Cushing's syndrome occur due to excessive secretion of ACTH from the pituitary adenomas, it is evident that only 10 15 % pituitary adenomas secret excessive ACTH. Even though approximately 10 % cases of the Cushing's syndrome occur due to excessive secretion of cortisol from the adrenal adenomas, it is evident that only 6 % adrenal adenomas secret excessive cortisol. However, exact aetiology of excessive secretion of ACTH from pituitary adenomas and cortisol secretion from adrenal adenomas has not been well established. Genetic studies established that mutation in the ubiquitin-specific protease 8 is responsible for Cushing's disease 1,2. Difference between Cushings syndrome and Cushings disease: Tumor in the adrenal gland produces more amount of cortisol. This leads to the development of Cushings syndrome. Cushings syndrome can also be developed due to tumor in the pituitary gland. Cushings syndrome is the group of symptoms in which cortisol levels remains elevated for the longer duration. Tumor in the pituitary gland produces more amount of ACTH. This ACTH stimulates more secretion of cortisol from the adrenal gland. This type of Cushings syndrome is called as Cushings disease. Tumors produced by ACTH can be produced anywhere in the body and these are termed as ectopic tumors. Long term steroid administration is one of the causes of Cushings syndrome. Cushings disease may occur due to the endogenous factors like self-overproduction of cortisol by the body. Endogenous over-production of cortisol may occur due to pituitary tumor (Cushings disease), adrenal tumor and ectopic tumors3. Hypothalamus is the part of brain below which pituitary gland is present. Corticotropin-releasing hormone (CRH) is secreted by paraventricular nucleus (PVN) of the hypothalamus. CRH stimulates pituitary gland to secret ACTH. ACTH gets transported through blood and as result adrenal gland gets stimulated to secret cortisol. Zona fasciculata is the region of cortex of adrenal gland which is responsible for the secretion of cortisol. Corticosteroid hormones are under the control of hypothalamus-pituitary-adrenal axis. Corticosteroids exhibit most prominent metabolic activity during the postprandial period. During this period, these hormones behave as contra-insular hormones. Hence, it provides substrates for oxidative metabolism and stimulate lipolysis and proteolysis. This results in the release of fatty acids and amino acids which induce glucose production by stimulating gluconeogenesis and inhibiting glycogen synthesis. Elevated levels of cortisol are responsible for the negative fee dback which is responsible for the reduced secretion of ACTH. Pathophysiology: In all types of etiologies of Cushing syndrome, there are raised levels of cortisol. Cortisol secreting adenoma in the cortex of adrenal gland occurs in Cushings syndrome. This adenoma of cortex of adrenal gland might be of primary hypercortisolism or hypercorticism types. Cushings syndrome due to elevated levels of ACTH is known as ectopic Cushing syndrome. Patients with severe hypercortisolism are associated with the phenotypes like glucose intolerance, dyslipidaemia, metabolic bone disease, and abnormal weight gain. On the other hand patients with mild or moderate hypercortisolism are rarely associated with glucose intolerance, dyslipidaemia, metabolic bone disease, and abnormal weight gain. Hence, it would be difficult to differentiate these patients from other patients with metabolic syndrome. There is presentation of striae, supraclavicular fat pads, and proximal muscle weakness in patients with increased hypercortisolism6. Elevated levels of corticosteroids results in the augm ented production of glucose at the level of liver and skeletal muscle. In liver corticosteroids increase levels of glucose by stimulating gluconeogenesis and inhibiting insulin sensitivity. Corticosteroids stimulate gluconeogenesis by acting on different genes responsible for glucose metabolism. Corticosteroids reduce insulin sensitivity by exerting antagonistic effect on metabolic action of insulin which is most important hormone required for suppression of glucose production7,8. Corticosteroids decrease expression and phosphorylation of insulin receptor substrate (IRS)-1, phosphatidylinositol-3kinase (PI3K) and protein kinase B (PKB/AKT). As a result, there is decrease in migration of glucose transporter GLUT4 to the cell surface which results in the reduction of glucose uptake. It also leads to decrease of glycogen synthase kinase (GSK)-3 phosphorylation and results in the decrease of glycogen synthesis. In skeletal muscles, corticosteroids increase insulin resistance which results in the decreased glucose uptake and prevention of glycogen synthesis. Corticosteroids exhibit effect on insulin resistance by directly acting on the insulin receptor or alteration in the insulin function by altering lipid and protein metabolism9,10. Corticosteroids also play prominent role in the regulating adipose tissue differentiation, distribution and metabolism. Corticosteroids can stimulate differentiation of pre-adipocytes in adipocytes. Increased adipocytes are associated with raised body fat mass. Corticosteroid specifically act on visceral fat and not on the peripheral fat. Hence, corticosteroids are associated with central obesity in Cushings syndrome. Corticosteroids also play role in the release of hormone like adipokine which is responsible for the development of insulin resistance. Co-occurrence of insulin resistance and increased visceral fat can lead to the development of metabolic syndrome which is associated with impairment in the glucose metabolism. Metabolic syndrome comprises of visceral obesity, diabetes mellitus, and dyslipidemia. Effect of corticosteroids on the pancreatic beta cells result in the decreased insulin secretion. Corticosteroids exhibit effect on insulin secretion in dose dependent and time dependent manner. Corticosteroid exhibit effect on different steps of insulin secretion like glucose uptake, glucose utilization and calcium fluxes and exocytosis of granules containing insulin. Glucose transporter GLUT2 and glucokinase expression gets reduced due to corticosteroids11,12. Corticosteroids can change AMP-activated protein kinase (AMPK) activity in tissue specific manner. Suppression of AMPK is proportional to hypercortisolism. Due to tissue specific activities, AMPK increases appetite, visceral obesity and dyslipidemia. Upon activation, AMPK plays key role in glycolysis and fatty acid synthesis which produces ATP. Due to hormone-sensitive lipase (HSL), there is increased level of lipids form adipose tissue which lead to development of adipocytes. 11 - hydroxysteroid dehydrogenase type 1 (11 H SD1) is responsible for the activation of cortisol from the inactive cortisone. 11 H SD1 overexpressed in mature adipocytes in conditions like hepatic steatosis and there is increased levels of cholesterol and triglycerides. 11 H SD1 is also associated with insulin resistance. Cardiovascular complications associated with corticosteroids include systemic arterial hypertension, atherosclerosis, and thromboembolism. It has been established that elevated levels of corticosteroid can lead to the increase in renin-angiotensin system, stimulated sympathetic nervous system and endothelin system. It also leads to reduced nitric oxide (NO) synthesis and kallikrein-kinin system. Patients of Cushings syndrome are associated with irreversible arterial stiffness. Endothelin, homocysteine, vascular endothelial factor, adrenomedulin, and cell adhesion molecules are the markers of endothelial dysfunction and are responsible for vascular endothelial and smooth muscle proliferation and fibrosis around vessels and consequently development of atherosclerosis plaques. In subclinical Cushings syndrome both systolic and diastolic hypertension can occur. Blood pressure can elevate in patients with Cushings syndrome due to ACTH stimulated cortisol level15,16. Corticosteroids also p roduces immunosuppression and neuropsychiatric complications. Ectopic ACTH production lead to Cushings syndrome and neurocognitive impairment. Neuropsychiatric disorders associated with Cushings syndrome are major depression, mania, anxiety, and cognitive impairment17. Bone complications associated with corticosteroids include osteoporosis and osteoarthritis. Osteoporosis may occur in patients with Cushings syndrome due to increased bone reabsorption, decreased bone formation, reduced intestinal calcium absorption and increased urinary calcium excretion18. Molecular Pathology: Adrenocortical carcinomas are associated with clinical hypercortisolism and androgen overproduction. Elevated levels of urinary metabolites of androgens or glucocorticoid precursors are evident in the adrenocortical carcinomas. It reflects reduced activity of steroidogenic enzymes. Bilateral macronodular adrenal hyperplasia (BMAH) is seldom connected with MEN1, familial adenomatous polyposis, and fumarate hydratase gene mutations. Bilateral adrenal hyperplasias are presented as in the form of nodule diameter greater than 1 cm (macronodular) or less than 1 cm (micronodular). Patients with Cushings syndrome possesses ARMC5 gene mutations and associated with subclinical BMAH. In addition to the ARMC5 gene mutation, there is occurrence of mutations in histone H3 lysine 79 methyltransferase gene (DOTL1), in a histone deacetylase gene (HDAC9), or in a prune homologue 2 gene (PRUNE2) in BMAH19,20. Molecular genetic abnormalities are helpful in the identifying causes of the Cushings syndrome. Glucocorticoid receptor gene mutation, dysfunction of proteins related to glucocorticoid-receptor function (Brg1 and HDAC2), and TP53-inactivating defects are responsible for the occurrence of Cushings syndrome. Overexpression of testicular orphan receptor 4 (TR4),30 a nuclear receptor with unknown ligand, the pituitary transforming gene (PTTG),31 and epidermal growth factor receptor are responsible for occurrence of Cushings syndrome. Overexpression of these genes are useful in identifying causal relationship and establishing therapeutic roles. Somatic mutations in the ubiquitin speci?c peptidase 8 gene (USP8) established role of epidermal growth factor receptor in Cushings syndrome. USP8 inactivation produces augmented epidermal growth factor receptor deubiquitination which leads to impairment in its down regulation and increased growth factor signalling and pro-opiomelanocortin (POMC) a nd ACTH synthesis. Mutations in the cAMP-dependent or -catenin signalling pathways are expresses in the adrenal adenomas. Mutations of GNAS (encoding Gs, which activates adenylate cyclase) are reported in cortisol secreting adenomas and -catenin (CTNNB1) mutations in cortisol-secreting adenomas. Protein kinase A (PRKACA) mutations are reported in adenomas of Cushings syndrome. Phosphodiesterase 11A (PDE11A) or phosphodiesterase 8B (PDE8B) genetic variants are responsible for adrenal adenomas21. Most of the clinical features of Cushings syndrome like body weight gain and blood pressure are common. Hence, it would be difficult to make exact diagnosis of Cushings syndrome. Hence, laboratory tests need to be performed for the diagnosis of Cushings syndrome. These tests would also be helpful in identifying Cushing disease which mainly occurs due to tumor of pituitary gland. Dexamethasone suppression test and 24-hour urinary and salivary measurement for cortisol are useful for the confirmation of Cushings syndrome. Dexamethasone suppression test involves frequent administration of dexamethasone and continuous monitoring of cortisol and ACTH levels. In this test, if body is monitoring cortisol, there would be decrease in the cortisol level. However, in cases of Cushings syndrome, there would be increase in the cortisol level. This test is not always useful because other illness or condition may produce high level of cortisol. This condition is called as pseudo-Cushings states. Doc tors need to treat pseudo-Cushings states like depression. Post treatment, if there is no reduction in cortisol along with other physical worsening, Cushings syndrome would be confirmed. ACTH measurement in the blood can be useful in differentiating Cushings syndrome and Cushings disease. Blood ACTH levels would be less in cases of Cushings syndrome, however it would be normal or higher in cases of Cushings disease. This is because, blood ACTH levels would be less in patients with adrenal origin Cushings syndrome as compared to the other origin of Cushings syndrome. ACTH producing tumor from the pituitary origin can be differentiated from the other parts of origin by using inferior petrosal sinus sampling, or IPSS. In this test, small plastic tube need to be inserted in the right and left veins in the groin and attach them to the veins near the pituitary gland. Blood should be collected form these veins and other locations far from the pituitary. During this procedure, medications which increase ACTH levels from the pituitary need to be injected. ACTH levels produced near pituitary and far from the pituitary need to be measured to assess tumors produced by pituitary origin. Inferior petrosal sinus sampling (IPSS) is more reliable as compared to the dexamethasone suppression test. Magnetic resonance imaging (MRI) can also be used as a diagnostic tool for Cushings syndrome. In this test, contrast is useful for showing up tumor in the MRI scan. Identification of the definitive tumor along with positive dexamethasone suppression test would be useful in diagnosis of Cushings disease. In such cases, there is no requirement of IPSS test. In few healthy people, there may be abnormal area on the pituitary, which might resemble tumor in MRI, hence abnormality doesnt reflect occurrence of Cushings disease. In few cases, tumor may be too small to detect using MRI. Hence, absence of tumor should not exclude Cushings syndrome. Sodium and potassium levels can be increased in patients with Cushings syndrome, hence assessment of electrolyte balance can be used as a diagnostic tool23. Treatment and management: Main aim of the treatment of Cushings syndrome should be reduction in the level of cortisol. Treatment of Cushings syndrome may vary based on the cause of the disease. Corticosteroid medication use should be reduced. Dose of the corticosteroid should be reduced. However, reduced dose of corticosteroid should be useful in the management of chronic inflammatory disease. Non-corticosteroids drugs can be administered along with corticosteroids to reduce dose of corticosteroids. Use of corticosteroids should not be stopped abruptly because it may lead to decrease in cortisol levels. In patients with existence of tumor, surgery should be performed to remove tumor. Pituitary tumors can be removed by performing surgery through nose and neurosurgeon can perform this surgery. Adrenal gland tumors can be removed by standard surgical procedure and using minimally invasive surgical technique. After the completion of the surgery, cortisol replacement medications should be provided to the patients to maintain normal levels of cortisol. Cortisol replacement medications usually takes long duration to maintain normal level of cortisol. Radiation therapy should be provided to the patients, in whom surgeon cant remove tumor completely. Hence, in such cases radiation therapy should be used as an adjuvant therapy along with surgery. Radiation therapy should be used in patients in whom surgery can not be performed. Radiation should be given in little doses for a duration of 6 weeks. Stereotactic radiosurgery, which is also called as Gamma Knife surgery can also be used, in which large single dose of radiation should be given to tumor part with minimal exposure to the surrounding area. Medications to control cortisol levels should be administered to patients, whom are very sick and surgery can not be performed in such patients24. Ketoconazole, mitotane and metyrapone can be used to reduce excessive production of cortisol from the adrenal gland. It is evident that, Ketoconazole can reduce plasma cortisone, however it can not reduce plasma ACTH. Metyrapone exhibits its action by inhibiting 11-hydroxylase. Due to use of metyrapone, there may be increase in ACTH levels relative to the decrease in the cortisol levels. This may result in the stimulation of the adrenal androgen and increased mineralocorticoid production. Mifepristone is useful in the Cushings syndrome patients with diabetes and glucose intolerance. Mitotane exhibits its action by inhibiting 11-hydroxylase, 18-hydroxylase, 3-hydroxy-lase, hydroxysteroid dehydrogenase, and several cholesterol side chain cleavage enzymes. Mitotane exhibits adrenolytic action by binding its metabolite to the macromolecules in adrenal cortical cell mitochondria. This results in the cell destruction and cellular necrosis. Mifepristone does not reduce cortisol level; howev er it blocks action of cortisol on tissues. Pasireotide is useful in the Cushings disease because it reduces the ACTH secretion from pituitary tumor. This medication should be administered twice daily, if surgery can not be performed or in cases of unsuccessful surgery. If none of the treatment works, bilateral adrenalectomy should be performed. In bilateral adrenalectomy, there would be surgical removal of adrenal gland. This surgical intervention is useful in reducing excess levels of cortisol, however such patients require life-long cortisol replacement medications. Newer compounds like CDK2/cyclin inhibitor R-roscovitin (targeting PTTG overexpression) or ge?tinib, the epidermal growth factor receptor-tyrosine kinase inhibitor are responsible for the inhibition of corticotroph tumour growth. Hence, these compounds are helpful in the alleviate clinical and biochemical features of Cushings syndrome. Ge?tinib exhibits effect in Cushings syndrome by decreasing ACTH secretion in USP8-mutated human corticotroph cells26. Patients with Cushings syndrome should take care of their general health. They should take healthy diet and exercise on regular basis. High impact or heavy weight exercise should be avoided by patients with Cushings syndrome because bones might weaken in these patients. More amount of calcium and vitamin D should be administered to strengthen the bones. Patients with Cushings syndrome should quit smoking and avoid consumption of large quantity alcohol. Nurse should advise MV to follow-up regular basis. MV should inform doctor about adverse effects of medications. Nurse should advise MV to keep adequate supply of corticosteroids to avoid shortage. MV and her family members should be aware of evaluating and measuring blood pressure, blood glucose and body weight. Safe environment should be provided to MV because there is possibility of fall due to weak bones. Fall prevention strategies should be provided to MV. MV should wear identification mark for Cushings syndrome, hence other docto rs can identify her as patient. Nurse should encourage MV to verbalize feelings and concerns. MV and family members should adapt to the emotional instability and should cope with mood swings, irritability, and depression. Assurance should be given to MV that, physical changes occurred due to Cushings syndrome can be disappeared if cause of the disease treated. Weight gain and edema can be managed by consuming low carbohydrate and low sodium diet. Conclusion: Excessive exposure to glucorticoids results in mortality and morbidity due to Cushing's syndrome. Genetic and molecular studies established that primary adrenal lesions and ACTH secretion are responsible for the excessive secretion of cortisol. Biochemical and imaging diagnostic studies proved useful in differentiating Cushing's syndrome from Cushing's disease. Radiotherapy, drug therapy and surgical treatment improved management of patients with Cushing's syndrome. Management goals for the patients with Cushing's syndrome should be normal functioning of the hypothalamic-pituitary-adrenal axis, normal functioning of the pituitary gland, and evading of tumour recurrence. References: Duan K, Gomez Hernandez K, Mete O. Clinicopathological correlates of adrenal Cushing's syndrome. J Clin Pathol. 2015; 68(3):175-86. Prague JK, May S, Whitelaw BC. Cushing's syndrome. BMJ. 2013; 346:f945. doi: 10.1136/bmj.f945. Ritzel K, Beuschlein F, Berr C, Osswald A, Reisch N, Bidlingmaier M, Schneider H, Honegger J, Geyer LL, Schopohl J, Reincke M. ACTH after 15 min distinguishes between Cushing's disease and ectopic Cushing's syndrome: a proposal for a short and simple CRH test. Eur J Endocrinol. 2015; 173(2):197-204. Gallo-Payet N, Battista MC. Steroidogenesis adrenal cell signal transduction. Compr Physiol. 2014; 4, 889964. Raff H, Sharma ST, Nieman LK. Physiological basis for the etiology, diagnosis, and treatment of adrenal disorders: Cushings syndrome, adrenal insuf?ciency, and congenital adrenal hyperplasia. Compr Physiol. 2014; 4: 739769. Zografos GN, Perysinakis I, Vassilatou E. Subclinical Cushing's syndrome: current concepts and trends. Hormones (Athens). 2014; 13(3):323-37. Resmini E, Minuto F, Colao A, Ferone D. Secondary diabetes associated with principal endocrinopathies: the impact of new treatment modalities. Acta Diabetol. 2009; 46(8): 595. van Raalte DH, Ouwens DM, Diamant M. Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options? Eur J Clin Invest 2009; 3(9): 8193. van Raalte D, Nofrate V, Bunck M, Van Iersel T, Elassaiss Schaap J, Nssander U, Heine R, Mari A, Dokter W, Diamant M. Acute and two-week exposure to prednisolone impair different aspects of beta-cell function in healthy men. Eur J Endocrinol. 2010; 1(62): 729735. Pivonello R1, De Leo M, Vitale P, Cozzolino A, Simeoli C, De Martino MC, Lombardi G, Colao A. Pathophysiology of diabetes mellitus in Cushing's syndrome. Neuroendocrinology. 2010;92(1):77-81. Abraham SB, Rubino D, Sinaii N, Ramsey S, Nieman LK. Cortisol, obesity, and the metabolic syndrome: a cross-sectional study of obese subjects and review of the literature. Obesity (Silver Spring). 2013; 21(1):E105-17. London E, Lodish M, Keil M, Lyssikatos C, de la Luz Sierra M, Nesterova M, Stratakis CA. Not all glucocorticoid-induced obesity is the same: differences in adiposity among various diagnostic groups of Cushing syndrome. Horm Metab Res. 2014;46(12):897-903. Arnaldi G, Scandali VM, Trementino L, Cardinaletti M, Appolloni G, Boscaro M. Pathophysiology of dyslipidemia in Cushing's syndrome. Neuroendocrinology. 2010;92(1):86-90. Ferra F, Korbonits M. Metabolic comorbidities in Cushing's syndrome. Eur J Endocrinol. 2015;173(4):M133-57. Valassi E, Biller BM, Klibanski A, Misra M. Adipokines and cardiovascular risk in Cushing's syndrome. Neuroendocrinology. 2012;95(3):187-206. Luigi Petramala, D'Elia Lorenzo, Gino Iannucci, Antonio Concistr, Laura Zinnamosca, Cristiano Marinelli, Giuseppe De Vincentis, Antonio Ciardi, Giorgio De Toma, and Claudio Letizia. Subclinical Atherosclerosis in Patients with Cushing Syndrome: Evaluation with Carotid Intima-Media Thickness and Ankle-Brachial Index Endocrinol Metab (Seoul). 2015; 30(4): 488493. Starkman MN. Neuropsychiatric findings in Cushing syndrome and exogenous glucocorticoid Administration. Endocrinol Metab Clin North Am. 2013;42(3):477-88. Miklos Toth, Ashley Grossman. Glucocorticoid-induced osteoporosis: lessons from Cushings syndrome. Clinical Endocrinology. 2013; 79, 111. Lib R, Coste J, Guignat L, et al. Aberrant cortisol regulations in bilateral macronodular adrenal hyperplasia: a frequent ?nding in a prospective study of 32 patients with overt or subclinical Cushings syndrome. Eur J Endocrinol. 2010; 163: 12938. Ho? and J, Ho? and LJ, van Koetsveld PM, et al. ACTH-independent macronodular adrenocortical hyperplasia reveals prevalent aberrant in vivo and in vitro responses to hormonal stimuli and coupling of arginine-vasopressin type 1a receptor to 11-hydroxylase. Orphanet J Rare Dis. 2013; 8: 142. Andr Lacroix, Richard A Feelders, Constantine A Stratakis, Lynnette K Nieman. Cushings syndrome. Lancet. 2015; 386: 91327. Judith Lowitz, Margaret F. Keil. Cushing Syndrome: Establishing a Timely Diagnosis. J Pediatr Nurs. 2015; 30(3): 528530. Rajput R. Cushings syndrome An update in diagnosis and management. Journal, Indian Academy of Clinical Medicine. 2013; 14(3-4): 235-41. Barnett R. Cushing's syndrome. Lancet. 2016; 13;388(10045):649 Reincke M, Ritzel K, Owald A, Berr C, Stalla G, Hallfeldt K, Reisch N, Schopohl J, Beuschlein F. A critical reappraisal of bilateral adrenalectomy for ACTH-dependent Cushing's syndrome. Eur J Endocrinol. 2015;173(4):M23-32. Fukuoka H. New potential targets for treatment of Cushing's disease: epithelial growth factor receptor and cyclin-dependent kinases. Pituitary. 2015;18(2):274-8. Ragnarsson O, Johannsson G. Cushing's syndrome: a structured short- and long-term management plan for patients in remission. Eur J Endocrinol. 2013;169(5):R139-52.

Essay of Claim of Author

Essay of Claim of AuthorOne of the keys to getting an A in college, after taking a final exam, is knowing how to write a sample essay of claim of the author. If you don't know what you are doing you will waste time and your paper may be rejected. It's really easy to make an essay look like a bad one. I've seen so many that are submitted to colleges that sound terrible.In addition to writing an essay of claim of the author, you must also use your writer's skills and your writing style. Because a very few people know how to write an essay, if they don't use the proper type of language you can get your essay disqualified. Your writing style will show if you know how to use strong words, good grammar, and write with great clarity. You'll need to write an essay that makes the reader think. If you use the same type of language to start your essay that you would use to go into detail about a topic, it will show that you know how to use it to communicate.Make sure you have a different type o f person in mind when you read it. If you are talking about something you learned in school or from a book, you will need to use strong language and make a statement that will make the reader feel something. In your essay of claim of the author, you should use your reader's emotions to make a strong statement. Sometimes an emotional response can make a point clear. A very few will do this, but if you use a lot of words that make no sense, you will lose points on this aspect.Next, be sure you follow the format and paragraph that are used in the school you are going to. These paragraphs and formats are calling norms and will be found in every publication for which you submit your essay. Be sure you follow them and never create any essay of claim of the author that does not follow the norms. Youressay will be rejected if you don't.Get to the point. Many schools require essays to have facts, figures, and statements that are factual. When you read this in an essay of claim of the author, you can become very emotional because it is important that you present facts and figures in a way that will tell the reader something. This part of your essay needs to make the reader do something, and you want to make them feel something by providing them with information.Finally, don't forget to use the article format. You will find articles to be very well-known, and they are perfect for essay of claim of the author. You may get a letter grade, but an essay that uses the article format is much better than an essay that doesn't.Don't let your lack of writing skills ruin the essay of claim of the author that you are submitting. Always remember to use strong language, build your emotions, and follow the norm of the school where you are writing.

Caesar Essays - Cleopatra, Julius Caesar, Julio-Claudian Dynasty

Caesar Expository Essay The decisions that one man makes can determine the length of life. Rome has many people that have the characteristics to be great leaders. Antony is a manipulative man, Brutus is an honorable man, and Octavius is a quiet strength. All three men would do an excellent job in leading Rome. Antony is a manipulative man. This is shown throughout the play in several cases, but most prominently at Caesar's funeral. ?I thrice presented him a kingly crown which he did thrice refuse. Was this ambition (III, ii, 96-96). Antony is very cleaver in the way that he presents his case to the people. He uses rhetorical questioning to show the people that Caesar was in fact not ambitious. Antony also played on the people's greed, to influence them to his side. ?I found it in his closet; ?tis his will/and they would go kiss Caesar's dead wounds (III, ii, 129, 132-133). Antony is very smart in the way he does this. He knows how to talk to the people to get them to believe his side of the story and revenge Caesar's death. Likewise, Antony is conniving. He uses this strength by flattering Brutus, and falsely befriending the conspirators into letting him speak at Caesar's funeral. ?I doubt not of your wisdom. Let each man render me his bloody hand.? (III, i, 200-201). Antony presents his c ase in such a way that Brutus and the other conspirators think that he is on their side, when in fact he really is going to turn the common people against them to revenge Caesar's death by creating a war. Furthermore, Brutus is an honorable man giving him the chance to be a great leader. Brutus is an idealist man, who is optimistic about assassinating Caesar. ?Grant that, and then is death a benefit. So are we Caesar's friends (III, i, 115). Brutus believes that with Caesar gone, Rome will greatly benefit. The common people will not be treated like bondsman, and Rome will not have someone who is driven by ambition to take over their country. Additionally, Brutus is also a noble person. Brutus helped in the assassination of Caesar not for personal gain but for the love of Rome. ?Not that I loved Caesar lee, but that I loved Rome more.? (III, ii, 21-22). Brutus is able to satisfy that his motive is pure; that his action is without bitterness and that the assassination of Caesar is for the general good of Rome. Brutus is also rigidly mortal. ?I did send to you For certain sums of gold, which you denied me, For I can raise no money by vile means. By heaven, I had rather coin my heart And drop my blood for drachmas than to wring From the hard hands of peasants their vile trash By any indirection. I did send To you for gold to pay my legions, Which you denied me.? (IV, iii, 78-86) Brutus is distressed with Cassius because he is led to believe that Cassius is accepting bribes, and denying Brutus the proper money to pay his troops. Brutus confronts Cassius and tells him that he was wrong to misuse his power and be so dishonest. Brutus clearly states that he loved Rome more than he loved Caesar, which in turn keeps his motives pure and his reasons for helping in the assassination honorable. Above and beyond, throughout the play Octavius is seen as a silent character, yet shows his strengths in several matters. Octavius is seen to be ill tempered. Though he is a quiet man if challenged he will take action. ?I do not cross you; but I will do so.? (V, I, 21). Octavius has much respect for Antony, however if he is challenged, or forced to do so he will cross Antony. This shows us that Octavius will stand up for himself and what he believes in. In addition, Octavius is respectful. ?Within my tent his bones to-night shall lie.? (V, V, 83). Octavius is referring to Brutus' dead body, when he recites these lines. He states this because he has the utter most respect for Brutus and what he stands for. Octavius believes Brutus is a man of importance and one to be honored, so he is going to honor him properly.

Impossible Nest Pas Français

Impossible N'est Pas Franà §ais The French expression impossible nest pas franà §ais is actually a proverb, equivalent to theres no such thing as cant or simply nothing is impossible. In French, you should never say that something is impossible, because, according to the proverb,  impossible isnt even a French word. Likewise, in English, you should never say that you cant do something because the concept of cant doesnt exist. In other words, nothing is impossible and there isnt anything you cant do. It would make a good motivational poster in either language (if youre into that kind of thing). Expression: Impossible nest pas franà §aisPronunciation: eh(n) puh seebl nay pa fra(n) sayMeaning: Theres no such thing as cantLiteral translation: Impossible isnt FrenchRegister: normal Example Tout le monde mavait dit que cà ©tait impossible  ; moi, je leur ai rà ©pondu qu «Ã‚  impossible nest pas franà §ais  Ã‚ » et puis je lai fait. Everyone told me you cant do that; I told them that theres no such thing as cant and then I did it.

Dances With Wolves Essay Example | Topics and Well Written Essays - 750 words

Dances With Wolves - Essay Example The mule wagon driver and a fort commander are odd personalities; the fort commander commits suicide after he sends Dunbar to his post, so no one is aware that Dunbar is on his legitimate duty. He mans the post alone after finding it deserted, gradually making friends with nearby Sioux villagers. In yet a different suicide incident, a Sioux lady cuts her wrists mourning her husband but Dunbar stops her. She is a white lady who was raised in the village. She becomes Dunbar’s interpreter and they ultimately fall in love The Sioux, the Pawnee and the white’s are all seen as having a conventional despise and hatred of people of other races. There is a great deal of violence: Indian on Indian, Indian on white, white on Indian, and white on white. The Sioux are humanized by being shown all through their lives; hence the viewers’ sympathy stays with them in their wars against the Pawnee, who are depicted as raiders and warriors (Monroe 167). Dunbar and his interpreter g irlfriend are shown making love while she is technically still mourning her husband. The Sioux are shown in a spectacular filmed buffalo hunting were the whites slaughter a lot of buffalos for just their tongues and skin. On contrary the Sioux could not waste any part of a buffalo, even when using insulated stomachs of the buffalos to cook as vessels to carry fire or as pots to cook, while some whites shoot the buffalos from train for pleasure just to see them fall. The federal soldiers are seen committing cruel acts on animals, and are classified as just plain crude (Hunter 98). Watching this film automatically arouses some Whiteman’s guilt (especially when if you are a white) and makes you more sensitive about treating any human being worthy of respect. When the film was first shown on a TV, some vulgar language were curled, but the out footage of with extra violence was added into it making it a four hour, two night mini-series. John Dunbar, a survivor of the civil war wit h a little knowledge of the American frontier and the plight of the Native Americans who inhabit it, acts as the role model of the film. He is open in different ways of life and he is smart, brave, heroic and loyal. Most the native Americans are shown as committed to their families, protect their way of living, eager to laugh, and live in harmony among themselves, an enormously different picture for this people in many other movies that came before this (Kevin Costner 112). With the Dunbar the only exception the other white soldiers are depicted as arrogant, ignorant and brutal. Intensively violent battles scene between the Native Americans and the white soldiers and between different native tribes are very common in the flow of the movie. Both innocents including children and the participants are shot with guns and or arrows. They are killed with hatchets, knifed, scalped or in furious hand to hand combat. Animal and human blood flows through out. Many animals including dogs, horse s and buffalos are attacked and shown bleeding or dying. On the hand the Indians ravage an innocent group of settlers: white soldiers pummel, beat and ferociously kicks the film hero; they also gleefully attack his beloved wolf for the sport of it. Violence is being used as the main theme of the movie though it does not seem to solve the problem. Indians get a