The Life Beathoven essays

The Life Beathoven essays I sit here listening to Beethovens Symphony No. 5, and wonder who this man was. I went to Ask.com, and asked whom he was, and they had a brief overview of the man. Beethoven, Ludwig van The composer of some of the most influential pieces of music ever written, Ludwig van Beethoven created a bridge between the 18th-century classical period and the new beginnings of Romanticism, ...and did much to enlarge the possibilities of music and widen the horizons of later generations of composers.(unknown author) His greatest breakthroughs in composition came in his instrumental work, including his symphonies. They think he was born Dec. 16 1770 in Bonn, Germany, and baptised on Dec. 17, 1770, the eldest son of a singer in the Kapelle of the Archbishop- Elector of Cologne, and grandson of the Archbishop's Kapellmeister, His father and grandfather worked as court musicians in Bonn. Ludwig's father, a singer, gave him his early musical training. I searched the ISU encyclopedias on his music, and realized that he had a predecessor, Wolfgang Amadeus Mozart, for whom writing music seemed to come easily, Beethoven always struggled to perfect his work. Beethoven had only meager academic schooling, he studied piano, violin, and French horn, and before he was 12 years old he became a court organist. Ludwig's first important teacher of composition was Christian Gottlob Neefe. In 1787 he studied briefly with Mozart, and five years later he left Bonn permanently and went to Vienna to study with Joseph Haydn and later with Antonio Salieri. Beethoven's first public appearance in Vienna was on March 29, 1795, as a soloist in one of his piano concerti. Even before he left Bonn, he had developed a reputation for fine improvisatory performances. In Vienna young Beethoven soon had a long list of aristocratic patrons who loved music and were eager to help him. Something that surprised me and about Beethov ...

College Life Essays - English-language Education, Free Essays

College Life Essays - English-language Education, Free Essays he ideal college lifestyle dissipates quickly once the reality is reached. Many young adults imagine vivid pictures of what college might be like for them. However, once these young adults mature into independent men and women, and enter into the school of their choice, they soon realize the reality of the college lifestyle. They must learn to adapt to their new surroundings as quickly as possible to accomplish the sought after degrees. Students come to the realization that life is not as easy as they might hope for. Many young adults seem to believe that college life is filled with parties and typically a laid-back lifestyle. These students believe that, much like high school, classes will be taken during the day and filled with all their friends. They imagine a lifestyle with no other worries besides an occasional essay or lab. It is often said that college is the greatest time of ones life; many high school students believe this and look forward to it. Some enjoy the idea of being able to come to class late, leave when they want, and pretty much have say-so of their own lives now that their parents are out of the picture. The majority of college freshmen enter into school picturing an easy, fun-filled ride. These reasons provide support to the unusually low grades of first-year college students. The widespread college ideal lifestyle is seldom the reality. Students quickly learn that many classes stretch into the nighttime hours. Often, students are not in classes with their friends, but with other students who sometimes can be old enough to be their parents. Although the average college age might be near 20 years old, it can range from 18 to 40 years old or older.

Database Applications Essay Example | Topics and Well Written Essays - 500 words

Database Applications - Essay Example A data mart is an easy data warehouse that focuses on one area of functionality or subject like finance, marketing and sales. A single department builds and controls a data mart for the whole organization. The sources of data mart ranges from external data, central data warehouse to operational systems. The implementation of a data mart takes place in a series of steps. The first step involves the designation of the schema that initiates the data request. The construction of the physical storage before populating the data mart with source systems data follows. One then accesses the data for initiating sound decisions. Finally, there is the management of data over time. Data mining analyzes data from diverse perspectives before summarizing it into useful information. Useful information is capable of minimizing costs and increasing revenue or doing both. The analysis of data requires the application of data mining software as an analytical tool. Data mining ensures analysis of data from different angles and dimensions. It also helps in categorizing and shortening the relationships of the data identified. Data mining seems to be a new term though it is not technologically. Over the years, many companies have applied the technology of data mining to sort through through supermarket scanner volumes besides conducting market research data analysis. Business intelligence is a blanket description of all the software applications use in the analysis of the raw data of an organization. The discipline of business intelligence comprises of reporting, online analytical processing, data mining and querying. It plays a crucial role in the improvement of decision-making, cutting costs and the recognition of new business opportunities by enterprising organizations. Besides, it can help the management of business organizations in the identification of those business

Summary of the Article - Government and Poverty Research Paper

Summary of the Article - Government and Poverty - Research Paper Example In the scenario, the author also makes a mention of the more recent American Recovery and Reinvestment Act. The author defines poverty as the dearth of the necessary resources that enable the people to meet their basic needs and extends the commensurate statistics regarding the urban, suburban and rural incidence of poverty. The author does support the extension of government aid to the deserving, while taciturnly mentioning that many people suffer from poverty because they are lazy. The writer also blames the indulgence in substance abuse like tobacco and alcohol as the reason as to why the poor remain poor. Yet, the writer again contradicts one’s assertion by saying that a great number of the poor receiving the government aid do tend to be employed. In the end, the writer conclusively asserts that the government should spend money on imparting skills and education to the poor, rather than wasting the taxpayers’ money on extending nutrition, health and housing. Overall the approach of the writer seems to be discernible against the government funding of the poverty alleviation programs. The poor tend to remain poor because they simply do not have a place in the national financial chain and many times, as said by the author, they lack the skills, education and connections to be able to fit into the national financial dynamics. Hence the government spending on the poverty alleviation programs is the most efficient way to make way for the allocation of the national wealth in favor of the impoverished segments of the society. The government has a self-interest in doing so in the sense that allowing the poverty to rise beyond a certain limit could lead to an unstable society marred by political unrest and crime (Lal & Myint 8). It is rightly said that the hungry minds are angry minds. Hence, state expenditure in poverty alleviation programs allows the government to channelize the skills, abilities and energy of poor sections of the society towards self-development and nation-building. State sponsoring of the poverty alleviation programs is not a choice but an important n ecessity and requisite. Hence, there is no scope or possibility for casting doubts on the relevance or necessity of the government spending on the poor or poverty alleviation programs. The writer himself conveyed that a majority of the poor people receiving government help does have jobs and they tend to work. Hence, the tongue in cheek assertion that the poor people are poor because they happen to be lazy is utterly nonsensical and biased. Poor people, in fact, happen to be poor because they do not have a say in the national and international policy-making procedures and frameworks, where they could chalk out the apt policies that would help them have a share in the process of wealth generation and allocation (Global Issues 1).

Health Care Administration Essay Example | Topics and Well Written Essays - 2500 words

Health Care Administration - Essay Example The current reform efforts in health professions education also focus on instructing members of the health care profession to work in interdisciplinary teams. This entails collaboration and integration of services and expertise in order â€Å"to ensure that care is continuous and reliable† (Peterson, 2003). Employing evidence-based practice, according to IOM, involves integration of best evidence and researches with clinical practice in order achieve optimum care for the patient. This encourages various health care students and professionals â€Å"to participate in learning and research activities to the extent feasible† (Peterson, 2003). The IOM also discussed that health professions education integrate quality improvement practices into health care practice. This involves having to identify the different errors and dangers in care, understanding safety design principles, â€Å"continually understand[ing] and measure[ing] quality of care in terms of structure, process , and outcomes in relation to patient and community needs†(Peterson, 2003). Finally, according to the IOM, members of the health care profession should be instructed on the use of informatics. This will help ease communication, easily manage data and information, and mitigate errors in the practice. The past 50 years in American history have yielded various changes in the health care practice. The cost of healthcare and the increase in health care allocation by the government and various investors have given birth to various improvements and innovations in the rehabilitation and care of patients. These new technology and new medical practices however have yielded various issues on quality and effectiveness of health care. The 1990s have produced various studies and reports revealing that advances in medical practice have not improved the quality of health care services for Americans. Medical errors

Oral Script About Titanic Essay Example for Free

Oral Script About Titanic Essay Good morning to my teacher and fellow friends. Today I want to talk about the sinking of Titanic. RMS Titanic was a passenger liner that sank in the North Atlantic Ocean on 15 April 1912 after colliding with an iceberg during her maiden voyage from Southampton to New York City. The sinking of Titanic caused the deaths of 1,514 people in history. She was the largest ship afloat at the time of her maiden voyage. One of three liners operated by the White Star Line, she was built between 1909-11 by the Harland and Wolff Shipyard in Belfast. Her passengers included some of the wealthiest people in the world, as well as over a thousand emigrants from Britain,  Ireland,  Scandinavia  and elsewhere seeking a new life in North America. The ship was designed to be the last word in comfort and luxury, with an on-board gymnasium, swimming pool, libraries, high-class restaurants and opulent cabins. She also had a powerful wireless telegraph provided for the convenience of passengers as well as for operational use. Though she had advanced safety features such as watertight compartments and remotely activated watertight doors, she lacked enough lifeboats to accommodate all of those aboard. Due to outdated maritime safety regulations, she carried only enough lifeboats for 1,178  people – a third of her total passenger and crew capacity. After leaving Southampton, England on 10  April 1912,  Titanic  called at  France  and Ireland before heading westwards towards New York. On 14 April 1912, four days into the crossing and about 375 miles south of Newfoundland, she hit an iceberg at 11:40  pm. The glancing collision caused  Titanics hull plates to buckle inwards in a number of locations on her  starboard  side and opened five of her sixteen watertight compartments to the sea. Over the next two and a half hours, the ship gradually filled with water and sank. Passengers and some crew members were evacuated in lifeboats, many of which were launched only partly filled. Just before 2:20  am  Titanic  broke up and sank bow-first with over a thousand people still on board. Those in the water died within minutes from  hypothermia  caused by immersion in the freezing ocean. The 710 survivors were taken aboard from the lifeboats by the  RMS Carpathia  a few hours later. The disaster was greeted with worldwide shock and outrage at the huge loss of life and the regulatory and operational failures that had led to it. Many of the survivors lost all of their money and possessions and were left destitute; many families, particularly those of crew members from Southampton, lost their primary bread-winners. They were helped by an outpouring of public sympathy and charitable donations. Some of the male survivors, notably the White Star Lines chairman,  J.Bruce Ismay, were accused of cowardice for leaving the ship while people were still on board, and they faced social ostracism. The  wreck of the  Titanic  remains on the seabed, gradually disintegrating at a depth of 12,415 feet (3,784  m). Since its rediscovery in 1985, thousands of artifacts have been recovered from the sea bed and put on display at museums around the world. Titanic  has become one of the most famous ships in history, her memory kept alive by numerous  books, films, exhibits and memorials. That’s all. Thank you.

Pathophysiology of sepsis | Case Study

Pathophysiology of sepsis | Case Study Thomas, a 70-year-old man, admitted to hospital with a five-day history of coughing with yellow-green sputum, pyrexia, rigors, poor appetite, mild chest pain and increasing difficulty of breathing. The initial observations are: Neurological: Altered neurological status, GCS 11/15. Agitated and confused. Cardiovascular: Sinus tachycardia, HR 135bpm. Hypotension, 90/45 mmHg. Respiratory: Tachypnoeic, RR 35bpm. Decreased saturation while receiving 6L O2 through Hudson mask. Metabolic: Febrile, 39 degree Renal: Oliguric with 20ml/hr urine output. Indwelling catheter (IDC) was inserted. The blood test revealed that the patient was suffering from hypernatremia, hyperkalaemia, hyperglycaemia, elevated urea, poor creatinine, increased WCC and low platelet count. The ABG indicated that Thomas was experiencing combined respiratory and metabolic acidosis. Thomas was finally diagnosed as sepsis complicated by the right middle lobe streptococcus pneumonia. He required intubation and invasive ventilation support. In this case study, the pathophysiology of sepsis will be discussed and the mechanism of synchronised intermittent mandatory ventilation (SIMV) volume control ventilation mode will be explained. Sepsis is defined as the dysregulated inflammatory response caused by severe infection (Neviere 2015). It has the interchangeable definition as Systemic inflammatory response syndrome (SIRS) while the SIRS is resulted by a suspected or confirmed infectious source (Neviere 2015). The concept of SIRS was first introduced by the American College of Chest Physicians (ACCP) and Society of Critical Care Medicine (SCCM) in 1992 (Kaplan 2014). It is characterised by two or more following symptoms. They are fever of high than 38 degree or hypothermia; tachycardia; tachypnoea or partial pressure of arterial carbon dioxide (PaCO2) less than 32 mmHg; deranged white cell count of more than 12,000/Â µL or less than 4,000/Â µL (O’brien et al. 2007). Associated with Thomas’s symptoms, it is clear to see that he was definitely experiencing sepsis. It is because that he was febrile up to 39 degree, tachycardic with heart rate of 135 bpm, and had increased respiratory rate of 35bpm as w ell as the elevated leucocytes count of 14,000 per microliter. The clinical signs are related to the inflammation process which is activated by the body immune system. Due to the severe infection, a large number of proinflammatory mediators are released which in turn result in the serial inflammatory reaction and extensive tissue damage (Neivere 2015). It is reported that SIRS can lead to high mortality rate because of high occurrence of SIRS induced multiple organ dysfunction syndrome (MODS) (Singh et al. 2009). In the following paragraphs, the pathophysiology of sepsis/SIRS will be more comprehensively examined. The pathophysiology of SIRS is complex. There are a few elements that need to be emphasised. They are acute stress response, inflammatory process and cytokine storm. Firstly, stress response is the acute phrase reaction when the body tries to defence against the threatening triggers. Those triggers are also known as ‘stress’. Stress can be caused by daily life events, environmental factors or physical illness (Better Health Channel 2012). In Thomas’s case, the stress response is initiated by infection. Under the influence of stress, the body steady state is disrupted. To maintain the homeostasis, the stress response is activated to reverse the body balance and redistribute the oxygen and energy to maintain the function of vital organs (Kyrou et al. 2012). Hypothalamus plays a vital role in processing the distress signals (Seaward 2015). Once it senses the stress, it triggers the activation of sympathetic nervous system. The sympathetic nervous system then stimulates the adrenal gland to produce epinephrine. It is also known as adrenaline. The adrenaline can lead to increased heart rate and myocardial contractility; dilated pupils and bronchi; peripheral vasoconstriction; accelerated respiratory rate; decreased digestive activity and increased production of glucose from liver (Seaward 2015). In addition, stress can also activate another pathway of stress response. That is the hypothalamic-pituitary-adrenal (HPA) axis (Seaward 2015). It means the stress triggers the release of corticotrophin-releasing factor (CRF) from anterior hypothalamus. The CRF then promotes the pituitary gland to produce adrenocorticoid trophic hormone (ACTH). The ACTH stimulates the production of cortisol and aldosterone through the adrenal cortex. Those corticosteroids can result in increased metabolism, sodium and water retention (Seaward 2015). Therefore, it is obvious that Thomas was under the effect of stress. He was tachycardic, tachypnoeic and slightly hyperglycaemic due to the effect of sympathetic nervous response. He was oliguric because of the acute kidney injury secondary to the vasoconstriction. His hypernatremia status can be contributed by the impact of aldosterone. He had poor oral intake can be cause by the suppressed digestion function. Secondly, the inflammatory cascade plays an essential role in the pathophysiology of systemic inflammatory response syndrome. Sagy et al. (2013) summarised the inflammation mediator related mechanisms in the systemic inflammatory response. It is indicated that the excessive release of pro-inflammatory mediators result in the inflammation, inhibit the function of compensatory anti-inflammatory response, and compromise the immune system eventually (Sagy et al. 2013). Cytokines are the essential components of immune system. Bone et al. (1992) explained that the local cytokines are activated immediately after an insult in order to repair the wound and initiate the innate immune system. Because of the release of local cytokines, a small amount of cytokines go into the circulation. This promotes the production of growth factor and adhesion of macrophages and platelets to help with the recovery of the local damage. However, when the infection is severe and the homeostasis is unable to be restored, cytokine storm occurs. More specifically, cytokine storm is formed from a complex progression. Cytokines are made up by macrophages, monocytes, mast cells, platelets and endothelial cells, which are the initial immune defensive components (Plevkova 2011). The multitude of cytokines can soon induce the cytokine tissue necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1). Those two elements result in the removal of nuclear factor-KB (NF-KB) inhibitor. This in turn prompts the production of more proinflammatory mediators, such as IL-6, IL8 and interferon gamma (Plevkova 2011). In other words, cytokines stimulate the production of immune cells, which in turn induce more cytokines in the circulation. The cytokines have a great impact on the body, including direct or indirect contribution of mortality in SIRS. TNFa is discovered causing fever, abnormal haemodynamic values, low white cell count, increased liver enzymes and clotting problems (Jaffer et al. 2010). IL-1 is reported having connection with fever, haemodynamic abnormality, loss of appetite, general weakness, headache and neutrophilia (Jaffer et al. 2010). IL-6 is found having strong relationship with fever and impaired lung function as well as acting a determinant of severity of SIRS and mortality rate (Jaffer et al. 2010). The massive accumulation of cytokines can cause widespreading vasodilatory effect. It is because the cytokines stimulate the release of vasodilators such as nitric oxide (Sprague and Khalil 2009). Additionally, cytokines promotes adhesion of the immune cells and the endothelial cells, which in turn leads to leaky endothelium and loss of fluid from intercellular space to extracellular space (Sprague an d Khalil 2009). Moreover, the cytokines cascade can also lead to the clotting disorder. It is because of the high concentration of fibrinogen in the inflammation process (Esmon 2005). The fibrinogen is converted from thrombin, which is generated by tissue factor. Tissue factor is a substance that is expressed by the surface of white cell. It can also be induced by TNFa and endotoxin from the infection (Esmon 2005). The fibrinogen can be transferred into fibrin which in turn forms clots. As the excessive amount of fibrin in the inflammation status, it can result in extensive clotting disorder. To sum it up, it can be concluded that Thomas’s fever is highly likely related to the release of TNFa, IL-1 and IL-6. IL-1 could be one of the contributors of his poor appetite and elevated white cell count. IL-6 could worsen Thomas’s existing affected lung function. Thomas had increased white cell count can be contributed by the immune response and IL-1. The hypotension is related to the vasodilation effect. Due to the hypotensive, the kidney perfusion dropped and then led to the acute kidney failure and poor urine output. The acute kidney injury may affect the elimination of potassium so that Thomas was found having high potassium level. The low platelet count could be related to the massive production of cytokines and damaged endothelium. In the next section, the synchronised intermittent mandatory ventilation volume control will be explained as Thomas’s mechanical ventilation management. The synchronised intermittent mandatory ventilation (SIMV) is commonly used in ICU. With the volume control mode, the patient is given the ventilation support with a set tidal volume during the mandatory breaths (Deden 2010). To provide the effective ventilation support, there are a few specific values that need to be set up for the SIMV volume controlled mode. They are tidal volume and respiratory rate. The tidal volume refers to the amount of oxygen delivered by the ventilator or the amount of oxygen the patient breathes voluntarily. The respiratory rate is set up for mandatory breaths. In the SIMV volume controlled mode, the ventilation is trigger by the ventilator or patient self. It means the actual respiratory rate can be upon the preset rate (Goldsworthy and Graham 2014). There is a window of time for the ventilator to sense the patient’s inspiratory effort. This trigger window helps avoid the ventilator deliver the oxygen when the patient exhales (Deden 2010). If the p atient is able to trigger the ventilation within the time frame, the patient-triggered mandatory breath is induced. After reaching the demand tidal volume, the inspiratory phrase ends and expiratory starts. Between each mandatory breaths, the patient is able to initial own spontaneous breath, the breathing volume and length depend on the patient’s respiratory effort (Pierce 2007). If the patient is heavily sedated and unable to initiate the spontaneous breath within the trigger window, the machine-triggered mandatory breath will be activated to provide constant ventilation support according to the set respiratory rate and tidal volume (Deden 2010). Once the ventilator delivers the demand tidal volume, the inspiratory cycle ends and expiratory phrase starts until the next scheduled inspiratory cycle. If the patient’s attempt of breathing is not strong enough to trigger the patient-triggered mandatory breath, the assisted synchronised breath will be provided to achieve t he desired the tidal volume. Like the other mode, the inspiratory cycle ends once the set tidal volume is delivered (Deden 2010). It is believed that Thomas would be beneficial from the SIMV volume controlled mode. It is because that SIMV mode could help him reduce the work of breathing, especially when he was in the high energy-consuming septic status. In addition, due to the SIMV mode, the ventilator allows him to have extra breath to blow off the accumulative carbon dioxide. This can improve his acidosis. Moreover, because of the systemic inflammatory response syndrome and severe pneumonia, his lungs could be stiff and fragile secondary to the inflammation effect and accumulation of cytokines. The volume controlled ventilation acts as a protective strategy to avoid the ventilator related complications, such as volutrauma. It is recommended not to set the tidal volume more than 8-10ml/kg (Deden 2010). In conclusion, sepsis is a systemic inflammatory response syndrome resulted by the infection. The stress response, inflammation reaction and cytokines play essential roles in the progression of SIRS. As SIRS can cause high mortality rate, it is vital to control the infection and manage the widespreading inflammation as well as providing appropriate support to treat the symptoms. In Thomas’s case, the volume controlled synchronised intermittent mandatory ventilation would be the better option of managing his severe pneumonia and respiratory distress. Reference Better Health Channel 2012, Stress, viewed 12th March 2015, http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/stress Bone, RC, Balk, RA, Cerra, FB, Dellinger, RP, Fein, AM, Knaus, WA, Schein, RM Sibbald, WJ 1992, ‘Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine’, Chest, vol. 101, no. 6, pp. 1644-1655. Deden, K, 2010, Ventilation modes in intensive care, Dragerwerk AG C0. KGaA, Germany Esmon, CT 2005, ‘The interactions between inflammation and coaulation’, British Journal of Haematology, vol. 131, no. 4, pp. 417-430. Goldsworthy, S Graham, L 2014, Compact Clinical Guide To Mechanical Ventilation : Foundations Of Practice For Critical Care Nurses, New York, NY Jaffer, U, Wade, RG Gourlay, T 2010, ‘Cytokine in the systemic inflammatory response syndrome: a review’, HSR Proceedings in Intensive Care Cardiovascular Anaesthesia, vol. 2, no.3, pp. 161-175. Kaplan, LJ 2014, Systemic inflammatory response syndrome, viewed 19th March 2015, http://emedicine.medscape.com/article/168943-overview#a0101 Kyrou, I, Chrousos, Kassi, E Tsigos, C 2012, Stress, Endocrine physiology and pathophysiology, viewed 12th March 2015, http://www.endotext.org/chapter/stress-endocrine-physiology-and-pathophysiology/#h23 Neviere, R 2015, Sepsis and the systemic inflammatory response syndrome: Definition, epidemiology and prognosis, viewed 19th March 2015, http://www.uptodate.com/contents/sepsis-and-the-systemic-inflammatory-response-syndrome-definitions-epidemiology-and-prognosis O’brien, JM, Ali, NA, Aberegg, SK Abraham, E 2007, ‘Sepsis’, The American Journal of Medicine, vol.120, no.12, 1012-1022. Pierce, LNB 2007, Management of Mechanically Ventilated Patient, 2nd edn, Saunders Elsevier, London Plevkova, J 2011, Systemic inflammatory response syndrome, viewed 24th March 2015, http://eng.jfmed.uniba.sk/fileadmin/user_upload/editors/PatFyz_Files/Handouty/angl/Systemic_inflammatory_response_syndrome_2011.pdf Sagy, M, Al-Qaqaa, Y Kim, P 2013, ‘Definitions and pathophysiology of sepsis, Current Problems in Paediatric and Adolescent Health Care, vol. 43, no. 10, pp. 260-263. Seaward, BL 2015, ‘Physiology of stress’, Managing Stress, Jones Bartlett Learning, Burlington, MA. Singh, S, Singh, P Singh, G 2009, ‘Systemic inflammatory response syndrome outcome in surgical patients’, Indian Journal of Surgery, vol.71, no.4, pp. 206-209. Sprague, AH Khalil RA 2009, ‘Inflammatory cytokines in vascular dysfunction and vascular disease’, Biochemical Pharmacology, vol. 78, no. 6, pp. 539-552. 1 Ying Hu 76898