Health Care Reform Bill Essay Example | Topics and Well Written Essays - 1250 words

Health Care Reform Bill - Essay Example Health Care Reforms According to Swan and Haas (2011), PPACA initiatives listed were favored by several national reports. First, the healthcare reform bills were put in place to enhance transparency and integrity in the program. Secondly, ensure all Americans have access to quality health care. Thirdly, make considerations to the providers of health care such as the hospital workforce. Fourthly, provide for public health improvement and prevent chronic diseases. According to the Thomas official website (2011), employers were expected to provide their employees with health insurance or take the option of subsidizing their employees’ healthcare by paying the government. This was the healthcare reform bills as at 2009 while they were still pending. H.R. 3590 Senate Bill and H.R. 3962 House Bill were proposed to provide Patient Protection and Affordable Care Act and Affordable Health Care for America Act respectively. As healthcare responds to the trends in cost, there would be a continuous catalyze on distribution and supply of healthcare. Problems are argued to arise in the post reform era on management of the trends of cost by deflecting the distribution network downwards and that of the supply chain. For example, between 1960 and 2008 the national expenditure healthcare cost grew from $28 billion to $2.34 trillion at an average growth of 10% annually, (Obamacare, 2011). The main difference with the House bill was its lack of surtax on wealthy individuals. H.R. 3590 has been described as having slow effects on different reforms. For example, the individual mandate has been schedule for 2014, a delay of a year. In that, if an individual does not obtain insurance coverage, they will face a penalty of $750 individually or the options of paying 2% gross income depending on the greater option. Regardless of the employees not mandatorily responsible for provisions of insurance to their employees, they are likely to face the same effects. In support of the Senat e Bill H.R. 3590, legislators argued that consumers were to benefit through the protection from unjustly practices by insurance providers. Also, the major advantage of the passed bill was the health accessibility and affordability to a larger population. As such, these legislators argued that U.S. deficit as at 2020 was likely to have reduced by approximately $100 billion. However, despite the above advantages, different groups opposed these reforms. First, they argued that the health care quality will be affected negatively yet its costs would have been increased. Different representatives from the congress approximated that the cost of the law at $2.5 trillion at a span period of 10 years and as a result, U.S. will most likely get into higher debts as noted by Coleman, Checkland, McDermott & Harrison, (2011). The Senate Bill was opposed by few stakeholders in the healthcare such as health insurers who argued that the private insurers were expected to maintain a minimum of 8% in pr emiums. Secondly, they opposed it in recognition that there will be reduction of insurance costs among small businesses. Thirdly, according to the U.S. Chamber of Commerce there was lack of principles in the reform that affected health status, food and drugs cases and fragmentation in the market as such they opposed this bill. On the other hand, pharmaceutical industries, physicians and AARP went in favor of the

Why Should You Know the Research Behind Turmeric?

Why Should You Know the Research Behind Turmeric?Researchers from various fields such as chemistry, pharmacology, pathology, health sciences and nutritional studies are all trying to help the growing health awareness regarding turmeric. Turmeric is a tropical spice that is found in India, Southeast Asia, Africa and the Middle East. It is highly concentrated and is naturally found in the roots of a rhizome plant called the cilantro plant.From time immemorial people have been using it to treat ailments, internal illnesses, digestive problems, osteoporosis, cancer, parasites, diarrhea, peptic ulcers, headaches, migraine, several allergies, some neurological disorders, depression, asthma, psoriasis, rheumatism, toothache, high blood pressure, blood sugar control, chronic fatigue syndrome, diabetes and a host of other diseases. Studies show that turmeric can reduce inflammation, improve immunity, help fight against colitis, diabetes, dysentery, arthritis, inflammatory bowel disease, bronc hitis, coronary heart disease, hemorrhoids, acne, acne vulgaris, and some types of cancer. In clinical trials, those suffering from several chronic diseases showed an impressive response to this medicinal herb.Researchers are divided into different medical fields such as pharmacology, immunology, biochemistry, radiology, cardiovascular science, dermatology, oncology, gastroenterology, pediatrics, psychiatry, epidemiology, neurology, urology, obstetrics, pharmacology, and many more. Researchers have published thousands of papers on the uses of turmeric to treat numerous diseases and this article will focus on just one such condition. Research shows that turmeric can be used to treat malaria.The use of turmeric as a remedy is not new but the same has been adopted in the conventional medicine with many twists and turns in its history. A traditional Indian medicine, Ayurveda, has consistently promoted turmeric as a cure for all manner of maladies and conditions. Since it is a powerful a ntiseptic, it is regularly used in cleansing your entire bodyof unwanted germs and bacteria.A common infection known as the cold sore, or the common cold, is also treated using turmeric. Other diseases like malaria, dysentery, gastroenteritis, ringworm, bacterial vaginosis, HIV, sore throat, prostate infection, asthma, burns, fevers, athlete's foot, psoriasis, and tonsillitis have all been treated using the much-coveted curcumin.In order to prevent infections and its complications, many physicians now prescribe turmeric as a dietary supplement along with their usual medicines and to help maintain health. It is considered to be a very important part of modern medicine today.Here is a published research paper that clearly illustrates the efficacy of turmeric and is the scientific explanation of the reasons behind the popularity of turmeric in various fields of medicine today. It is well worth reading.

Purchasing Top College Essay Topics

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The Ultimate Essay Writing for Research Paper Trick

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Analysis of Medical Errors Research Paper Example | Topics and Well Written Essays - 3000 words

Analysis of Medical Errors - Research Paper Example   The issue is heavily laden with the emotional and fiscal burden as patients must be aware of their treatment progress and any mistakes that have been made while hospitals and doctors have a very real need to protect themselves from lawsuits and protect their credibility. At the same time, it is difficult for many doctors to have to face the fact that in the course of attempting to improve health, they may have inadvertently made it worse and then to try to communicate this failing to the patients who have trusted them. While it seems the greatest opinion among medical workers is that patients should be informed whenever mistakes have been made, the reality is that the medical profession has a large tendency to hide mistakes when possible so as to avoid unpleasantness.  Ã‚   In â€Å"Disclosing Medical Errors to Patients, †1 the authors point out the prevalence of avoidable error or ‘adverse events’ within the medical profession as being relatively high – 37 percent of the discovered cases in a Canadian study preventable. In response to this, â€Å"leaders in the patient-safety movement have called for the system defects that underlie most errors to be corrected, as well as improvement in the recognition and reporting of errors and the disclosure of harmful errors to patients and their families.†2 Benefits of full disclosure are outlined, such as patients having greater knowledge about their own treatment  and thus able to make more informed decisions and patients’ ability to participate in problem-solving techniques to prevent future errors from occurring again.  Ã‚  However, the article also points out the difficulty doctors have had in providing full disclosure.  Ã‚  

Sickle Cell Disease: Causes, Effects and Treatment

Sickle Cell Disease: Causes, Effects and Treatment Abstract Sickle cell disease is a genetically inherited hematological (blood) disorder that results from a mutation in the beta globin gene that is responsible for the development of hemoglobin. Hemoglobin is the protein that delivers oxygen to the red blood cells throughout the body. In the disease, a mutated variant of normal hemoglobin generates an abnormal structure of the cells, leading to the development of symptoms. Sickle cell anemia and beta thalassemia are two common types of sickle diseases that are discussed in this review. The symptoms, complications, and therapies are also highlighted in the context of the pathophysiology of the disease. Sickle Cell Disease: An Overview Sickle cell disease is a genetically inherited blood disorder and it is characterized by an abnormal structure or production of hemoglobin. Hemoglobin is the protein in red blood cells that transports oxygen to cells throughout the body (National Institutes of Health, 2014). The disease results from a mutation in the beta globin gene causing a class of sickle diseases, such as sickle cell anemia and beta thalassemia (Thein, 2008). Together, they are often referred to as the beta hemoglobinopathies and present a range in disease severity (Thein, 2008). Beta globin is a protein that produces hemoglobin and the gene mutation in both diseases produces abnormal variants of hemoglobin in the blood. This results in either a predominance of abnormal hemoglobin molecules in red blood cells or an absence of normal hemoglobin, and thus, normal red blood cells (Edwards et al., 2005). There are a number of available therapies that manage sickle cell disease and the only curative treatment is hema topoietic cell transplantation. Pathophysiology of Sickle Cell Disease The National Institutes of Health reports that sickle cell disease is the most common inherited blood disorder in the United States and it affects 70,000 to 80,000 Americans (National Institutes of Health, 2014). It is estimated to occur in 1 in 500 African Americans and 1 in 1,000 to 1,400 Hispanic Americans (National Institutes of Health, 2014). The disease affects 30 million people worldwide and it is most common among people who have ancestors from Africa, Mediterranean countries, the Arabian Peninsula, India, parts of South America, Central America and the Caribbean (Khoury, Musallam, Mroueh, Abboud, 2011; National Institutes of Health, 2014). As it is an inherited disease, the sickle gene is presumed to have a genetic advantage in which it protects from the development of malaria infection (Stuart Nagel, 2004). There are many types of sickle diseases, such as sickle cell anemia and beta thalassemia. Sickle cell anemia is considered the most commonly occurring type of sickle c ell disease (National Institutes of Health, 2014). In sickle cell anemia, hemoglobin S replaces both beta-globin and the sixth amino acid is changed from glutamic acid to valine (National Institutes of Health, 2014; Rees Gibson, 2011). Sickle cell trait is not considered a disease and it is found in approximately 1 in 10 African Americans (Edwards et al., 2005). When both parents have the sickle cell trait, there is a one in four chance with each pregnancy that the child will have sickle cell anemia (Edwards, et al., 2005). Today, many health organizations offer newborn screenings that can determine if a child has either the disease or trait (National Institutes of Health, 2014). The development of the disease occurs due to the polymerization of deoxygenated hemoglobin S (Chirico Pialoux, 2012). The polymer formation modifies the normal red blood cell disc shape into a rigid, irregular-shaped, unstable cell and causes intravascular hemolysis, or rupture of the cells, to release hemoglobin into the plasma of the blood (Chirico Pialoux, 2012). The repeated polymerization leads to sticky blood cells (blood cell adhesion), obstruction of blood vessels (vasocclusion), and restriction of blood supply to tissues and organs in the body (ischemia) (Chirico Pialoux, 2012). Additionally, the endothelium and leukocyte, or white blood cells, are also found to play a role in disease mechanisms. Studies have found a connection between the endothelium, a thin layer of cells that line the interior surface of blood vessels, and sickled red blood cells (Stuart Nagel, 2004). The red blood cell receptors that are associated with cell adhesion are present in increased numbers on sickled immature red blood cells and mature sickle cells compared to normal red blood cells (Stuart Nagel, 2004). This finding demonstrates a structure-function abnormal activity that leads to coagulation on cell surfaces, leading to anemia (Stuart Nagel, 2004). Like cell adhesion, leukocytes have an impact in disease activity. White blood cells are found to be at an increased baseline in sickle cell disease, which serves as an independent risk factor for pulmonary and cardiac complications (Stuart Nagel, 2004). The size of the white blood cell, its rigidity, and adhesive characteristics are implicated in microvascular blood flow, vascular inflammation, and vasocclusion (Stuart Nagel, 2004). Clinical Symptoms of Sickle Cell Disease The clinical manifestation of sickle cell disease can lead to inflammatory responses and may result in acute chest syndrome, pulmonary hypertension, and stroke (Chirico Pialoux, 2012). People with sickle cell disease may also encounter several physical complications, such as delayed growth, fatigue, headaches, and cerebral vascular damage (Edwards et al., 2005). Acute chest syndrome is considered the second most common cause of hospital admissions and a leading cause of death in patients with sickle cell disease (Khoury, Musallam, Mroueh, Abboud, 2011). It involves the presence of a pulmonary infiltrate on a chest X-ray and the symptoms may include chest pain, a temperature of more than 38.5 degrees Celsius (101.3 degrees Fahrenheit), tachypnea (rapid breathing), wheezing or cough ((Khoury, Musallam, Mroueh, Abboud, 2011). The symptoms at clinical presentation vary with age as wheezing, cough, and fever are common in children 10 years or younger (Khoury, Musallam, Mroueh, Abboud, 2011). Pain in the arms and legs and shortness of breath are more commonly presented in adults with the disease (Khoury, Musallam, Mroueh, Abboud, 2011). It is believed that there are three mechanisms involved in acute lung injuries, which include infection, fat embolization (clotting) from bone marrow, and sequestration of sickled red blood cells (Khoury, Musallam, Mroueh, Abboud, 2011). People with sickle cell disease have an increased risk for developing infections, particularly pneumonia. Treatment for acute chest syndrome is primarily supportive and includes supplemental oxygen to keep the saturation above 92% (Khoury, Musallam, Mroueh, Abboud, 2011). Pain is considered the most frequent complication associated with the disease and acute chest syndrome stimulates this crisis (Edwards et al., 2005; Khoury, Musallam, Mroueh, Abboud, 2011). Repeated episodes of acute chest syndrome predispose patients to chronic pulmonary disease, such as pulmonary hypertension (Stuart Nagel , 2004). The occurrence of asthma is also associated with the increased incidence of acute chest syndrome, which is considered a comorbid condition found in people with sickle cell disease (Khoury, Musallam, Mroueh, Abboud, 2011). Beta Thalassemia Beta thalassemia is a common genetic blood disease that reduces hemoglobin production (National Institutes of Health, 2014). The hemoglobin gene mutation results in an unusually low level of beta-globin (National Institutes of Health, 2014). There are different levels of thalassemia based on the number of copies of beta thalassemia alleles or different copies of the same gene (Thein, 2008). The variety in alleles impacts the deficit in beta globin production, which, in turn, impacts disease severity (Thein, 2008). Carriers, for example, who have inherited a single copy of the beta thalassemia allele are clinically asymptomatic and may demonstrate mild anemia (Thein, 2008). Unlike a globin imbalance that is found in sickle cell anemia, variants of beta chains are broken down and result in ineffective red blood cell production in beta thalassemia (Thein, 2008). Physical complications involve cardiac and bone disease, bilirubin metabolism, and iron metabolism. Such symptoms may include jaundice and a predisposition to gallstones (Thein, 2008). Treatment for Sickle Cell Disease Several complications may emerge from sickle cell disease, whether it is in sickle cell anemia or in beta thalassemia. The purpose of therapies for sickle cell disease is to prevent and treat complications (Inati, Chabtini, Mounayar, Taher, 2009). The treatment of sickle cell disease is best achieved by decreasing the amount of hemoglobin S through the prevention of its production (Inati, Chabtini, Mounayar, Taher, 2009). People with severe sickle cell disease are treated with three validated therapies: hydroxyurea, transfusion and chelation therapy, and a hematopoietic or stem cell transplant (Inati, Chabtini, Mounayar, Taher, 2009). Hydroxyurea has been shown to be an effective form of treatment for children and adults with the disease. It has been demonstrated to reduce pain and acute chest syndromes, and it decreases the frequency of hospitalizations and the need for transfusions. This therapy has also been found to play a role in stroke prevention (Inati, Chabtini, Mounayar, Taher, 2009). At a molecular level, hydroxyurea reduces the adhesion of sickle red cells to endothelial cells. It also modulates endothelial cell activation and nitric oxide generation (Inati, Chabtini, Mounayar, Taher, 2009). Nitric oxide has been found to affect acute and chronic complications of sickle cell disease (Stuart Nagel, 2004). Nitric oxide, on a normal functioning level, induces relaxation of smooth muscle and dilation of blood vessels. In sickle cell disease, the bioavailability of nitric oxide is impaired, resulting in an imbalance between endothelial production and consumption (Stuart Nagel, 2004). The lungs are most affected by a reduction of nitric oxide and tend to constrict, which predisposes an individual to acute chest syndrome (Stuart Nagel, 2004). No adverse effects have been thus far reported on the usage of hydroxyurea and any toxicity is typically reversible (Inati, Chabtini, Mounayar, Taher, 2009). Transfusion therapy is currently considered a standard of care treatment for primary and secondary stroke prevention in children with sickle cell disease (Inati, Chabtini, Mounayar, Taher, 2009). It is used for short and long term management, preventing a first stroke in high-risk children as well as preventing against a recurrent stroke (Inati, Chabtini, Mounayar, Taher, 2009). Transfusions are also used for chronic and severe pain or in cases when patients with acute chest syndrome do not respond to hydroxyurea (Inati, Chabtini, Mounayar, Taher, 2009). Chelation therapy is used for patients who experience iron overload. Iron overload is a serious and inevitable outcome from receiving regular transfusion therapy (Inati, Chabtini, Mounayar, Taher, 2009). Unless treated, iron overload may result in severe organ damage and other life threatening complications and this treatment mediates this by removing excess metals from the body (Inati, Chabtini, Mounayar, Taher, 2009). While hydroxyurea, tranfusions, and chelation therapy aim to prevent and treat complications, they do not cure sickle cell disease (Inati, Chabtini, Mounayar, Taher, 2009). The currently available curative treatment is a stem cell transplant. A transplant is indicated in those patients who experience complications, such as recurrent severe pain, acute chest syndrome, and stroke (Inati, Chabtini, Mounayar, Taher, 2009). Only one-third of affected children meet the criteria for a stem cell transplant as it is an aggressive and serious procedure (Inati, Chabtini, Mounayar, Taher, 2009). The goal of a stem cell transplant is to replace the host’s marrow with normal cells, resulting in a new immune system (Stuart Nagel, 2004). Studies on stem cell transplant as a curative option for patients with severe sickle cell disease are demonstrating mean overall survival and event-free survival rates between 95 and 85% (Inati, Chabtini, Mounayar, Taher, 2009). Significant advancements have been made for pediatric patients who have beta thalassemia and were treated with a stem cell transplant. Over the last three decades, disease-free survival rates have exceeded 80% in patients who received transplants from biologically compatible family donors (Mehta Faulkner, 2013). Sickle cell disease is a genetically inherited blood disorder that is primarily diagnosed in people who have ancestors from Africa, Mediterranean countries, the Arabian Peninsula, India, parts of South America, Central America and the Caribbean (Khoury, Musallam, Mroueh, Abboud, 2011; National Institutes of Health, 2014). The disease results by a mutation in the gene that creates beta globin, which is the protein that is responsible for producing hemoglobin. Hemoglobin is the protein in red blood cells that transports oxygen to the body’s organs and tissues. When the mutation occurs, a hemoglobin variant is produced, resulting in a structural and functional change in the red blood cells. Several physical complications emerge in both children and adults who have the disease. These may include, but not limited to, pain, acute chest syndrome, cerebral and vascular damage (Edwards et al., 2005). There are three primary therapies for managing and/or treating the disease. These inc lude the drug, hydroxyurea, transfusion and chelation therapy, and hematopoietic cell transplantation (Inati, Chabtini, Mounayar, Taher, 2009). More research is underway in the development of additional treatment options, such as gene therapy and clinical trials are exploring this possibility. References Chirico, E. N., Pialoux, V. (2012). Role of oxidative stress in the pathogenesis of sickle cell disease. International Union of Biochemistry and Molecular Biology Life, 64 (1), 72-80. Edwards, C. L., Scales, M. T., Loughlin, C., Bennett, G. G., Harris-Peterson, S., De Castro, L. M., Whitworth, E., Abrams, M., Feliu, M., Johnson, S., Wood, M., Harrison, O., Killough, A. (2005). A brief review of the pathophysiology, associated pain, and psychosocial issues in sickle cell disease. International Journal of Behavioral Medicine, 12 (3), 171-179. Inati, A., Chabtini, L., Mounayar, M., Taher, A. (2009). Current understanding in the management of sickle cell disease. Hemoglobin, 33 (S1), S107-S115. Khoury, R. A., Musallam, K. M., Mroueh, S., Abboud, M. R. (2011). Pulmonary complications of sickle cell disease. Hemoglobin, 35 (5-6), 625-635. Mehta, P. A., Faulkner, L. B. (2013). Hematopoietic cell transplantation for thalassemia: a global perspective BMT tandem meeting 2013. Biology of Blood and Marrow Transplantation, 19, S70-S73. National Institutes of Health (2014). Genetics home reference: beta thalassemia. U.S. Department of Health and Human Services, Retrieved from http://www.ghr.nlm.nih.gov/condition/beta-thalassemia. National Institutes of Health (2014). Genetics home reference: sickle cell disease. U.S. Department of Health and Human Services, Retrieved from www.ghr.nlm.nih.gov/condition/sickle-cell-disease. Rees, D. C., Gibson, J. S. (2011). Biomarker in sickle cell disease. British Journal of Haematology, 156, 433-445. Stuart, M. J., Nagel, R. L. (2004). Sickle-cell disease. Lancet, 364, 1343-1360. Thein, S. L. (2008). Genetic modifiers of the ÃŽ ²-haemoglobinopathies. British Journal of Haematology, 141, 357-366.

Theseus Or Hercules? :: essays research papers

Theseus or Hercules? Theseus is most worthy of emulation. He was a great hero in Athens. "Theseus was, of course bravest of the brave as all heroes are, but unlike the other heroes he was as compassionate as he was brave." (p. 159). Theseus also was a man of bravery, intellect and bodily strength. Hercules on the other hand was what all Greece except Athens most admired. He was very strong but wasn't too smart. Hercules never thought of the consequences that his actions would bring about before he followed through with them. First, Theseus was very strong. He fought many terrible horrendous monsters such as the Minotaur, "..a monster, half bull, half human.." (p.151), and went on many great ventures such as the Quest for the Golden Fleece. Theseus showed his great strength in adventures such as the one with the Minotaur. Hercules was also involved in many great adventures in which his great strength was shown. Hercules was much stronger than Theseus, but Theseus made up for this small loss in other ways. Second, Theseus was very smart. Because of his great intellect the Athenians, people who valued thought and ideas, chose him and not Hercules as their hero. Theseus escaped from the Labyrinth and killed the Minotaur. Neither of these tasks were easy and required someone with aptitude unlike Hercules. Theseus always thought things through and made good decisions. Hercules' foolishness was shown on many occasions such as when he killed his family and his music teacher. Theseus' intellect is one very valuable quality which makes him more worthy of emulation. Third, Theseus was very brave. In fact he went on so many great excursions that a saying grew up in Athens "Nothing without Theseus!" (p. 149). When it was time for Theseus to seek his father he would not go by water " But Theseus refused to go by water because the voyage was safe and easy." (p. 149). Theseus insisted to take the way by land. His idea was to become a hero as quickly as possible, and he accomplished his goal by ridding the land of all the banns to travelers on his way to find his father. Theseus had many other adventures. He was on the Argo, in the Caledonian hunt, as well as many others. Hercules also had many adventures but his were often the result of his own