Cognitive Process Culture Essay Example for Free

Cognitive Process Culture EssayLamadrid takes into account the mythological or magical dimension of the novel and relates it to the acclivitous social consciousness of the protagonist. He asserts that Anaya elucidates that the command of Curandera is consequential in nature is derived from mythical though process and it resultant knowledge. These mythical thought processes itself are derived from final result of the contradiction that is inherent within the culture. So he portrays power as capability to contemplate and comprehend the social processes in a dialectical way. So myth is not something extra-human and acultural phenomenon but it is a cognitive representation of social thought process. This scholarly clause facilitates readers to understand the role of Antonio in the context of mythical realism and development of his mature social consciousness at the end of the novel. People resort to Antonio at critical times because they are inherently cognisant that these mediat ors have powers that can offer remedies to their maladies. So myth helps understanding the role of Antonio in the society and how this role is established.Mancelos, Joao de. Witchcraft, Initiation and Cultural Identity in Rudolfo Anayas call forth Me, Ultima. Alfarrabio. Retreieved on 12 October 2008. Website http//alfarrabio. di. uminho. pt/vercial/zips/mancelos21. rtf This article manifests the development of Antonio and how different elements of chicano culture i. e. witchcraft, cultural identity play a vital role in percentage him achieving maturity. He considers the role of Ultima and his witchcraft prowess to help Antonio explore his cultural identity.This article elaborates the role of his familial traditions, by his Hispanic lineage and his Catholic piety at an early stage of his life. Later he learned the tussle between Ultima and his religions but prefers Ultima and his witchcraft. All this contribute toward his maturity at the end of the novel. This article explains va rious developmental stages of Antonio and contribution of various factors during these periods and enables us to understand the contributories toward this development.

Post-WWII History Essay Example for Free

Post-WWII History EssayAfter World War II, the join States focused on putting an end to communism. The frugal climate of the immediate postwar years was conducive to the rise of the political left. The detrimental effects of depression and global war gen erated popular demands for widespread social, political and economic reforms. Furthermore, wartime controls made ordinary citizens believe that economic planning was the best way to restore economic growth and equity (Painter, 1999). The United States, however, underwent a shift to the right.Republican domination of both houses of Congress after the 1946 midterm elections led to the strengthening of conservative foe to the New Deal. Despite this accomplishment, the Republicans were unable to contain the main achievements of the New Deal unionization of heavy industry, Social Security, agricultural subsidies and civil rights militancy. Throughout Europe and in parts of the Third World, meanwhile, chaotic social, political a nd economic conditions resulted in the emergence of Communist parties and other leftist groups (Painter, 1999).The aforementioned developments prompted Washington to assume that a sensitive foe was in its midst Communism. McCarthyism The Great American Red Scargon The period from the late 1940s to the mid-1950s was characterized with the rise of Communism in China and several(prenominal) nations in Eastern Europe. As a result, the US became fearful that it was losing the power struggle against the Soviet Union a battle that was later known as the Cold War. This apprehension was exacerbated by suspicions that traitors within the American government were aiding the spread of Communism (Fitzgerald 2006).Such paranoia on the part of the US eventually resulted in the era of McCarthyism, a chapter in American history that was synonymous with state-sponsored Communist witch-hunts and anticommunist hysteria among the populace. Red Alert On the night of February 9, 1950, a senator from Wi sconsin named Joseph McCarthy gave a Lincoln solar day speech to the Republican Womens Club of Wheeling, West Virginia. His speech on that particular evening, however, had absolutely nothing to do with Abraham Lincolns birthday.McCarthys turn to instead focused on the hostile relations between the US and the Soviet Union. He warned the audience that the Soviet Union intended to spread Communism throughout the US by sending spies to infiltrate the US government (Fitzgerald 2006). To prove this claim of his, McCarthy held up a piece of paper and reportedly verbalize I have here in my hand a list of 205 (men) that were known to the secretary of state as being members of the Communist Party and who, nevertheless, are still working and shaping the policy of the State Department.(p. 10) This was a very grave allegation. The State Department is the government institution responsible for the establishment of contrasted policy. The presence of Communists in such an important organization would therefore cripple the US in its fight against Communism worldwide. They would most likely work as spies, providing the Soviet Union with sensitive information about atomic weapons and US military and political strategy (Fitzgerald 2006).

Similarities between Christianity and Shinotoism

Similarities amongst deliverymanianity and ShinotoismUndoubtedly, a soul craving to comprehend the sacred and the religious has served as the drive for the sustained expansion and improvement of religious communication. Consequently, when a mortal reflects on the standard and range of the worlds religions, it is not shocking to discover that on that point atomic number 18 overabundances of religious principles that have been formed. Bearing this in mind, this analysis reflects on the capacities of religious inquisition that has been fashioned. Particularly, this analysis evaluates Christianity and Shintoism. Through a close reflection of what has been written regarding these religions, and through a personal interview that was conducted, it will be feasible to present an explanation of the backgrounds and similarities and departures of the religions.In order to start this analysis, it is first accommodating to think nearly the meaty background of some(prenominal) religi ons. First, examining the basic doctrines and evolution of Christianity, it blends app argonnt that this religion developed from the Jewish tradition as depicted in the Old Testament. The difference is, however that Christianity firmly believes in the resurrection of Jesus Christ. Christianity concerns the capacity of God to resurrect the dead, just like He did for Jesus. Through finding faith in Christ, the following are given the ability to guarantee that they could live a life that would give them aeonian salvation (New Advent, 2009). The New Testament offers detailed depictions of how Jesus lived and insights into his resurrection.When examining Christianity, it becomes actually clear that the magnitude of the resurrection is momentous to the development of the religion. In general, the resurrection is the most signifi shagt characteristic that expresses Christianity. Through the resurrection, a person is given salvation from God an eternal life. Even though the precise circu mstance of the resurrection is what separates Christianity Judaism, there is a drive to recognize why Christianity has become so dominant to its following. One of the reasons why it has become so dominant is the result of many of its chase believing that through faith, God will guard and supply.It is now obvious why Christianity is such a come uponed religion it is because of the assurances that it gives its followers. Every person goes into a covenant with God when s/he accepts the teachings of Christ (New Advent, 2009). Through this procedure, a person is assured to be given eternal deliverance for his or her labors in living a life that is based on the principles of Christ. Despite the consequences of how tricky life is, a person must constantly stick to the larger agenda of his teachings. By doing this, they will basically be resurrected in the afterlife (New Advent, 2009). The assurance of this resurrection gives the followers a imprint that life goes on after a person dies. In order to conduct my interview and obtain information about Shintoism, I decided to cause an Internet search to see where the closest Shino center was. It turned out the closes center was located at 300 W. 55th St, 20B, New York, NY which wasnt terribly intemperate for me to go to. It is called the International Shinto Foundation (New York Center). It was, however, very difficult for me to get in touch with a representative, so I decided to simply give a right smart an unannounced trip there in expectation that I would be able to speak to someone who had a strong grasp on Shintoism. My efforts were certainly rewarded I was able to connect with an English-speaking man who was responsible for maintaining the tea ceremony room. He gave me a great deal of valuable information, and it is with this information that I am able to offer a summary of the religion, in addition to being able to compare and contrast it to Christianity and draw up a conclusion.Shintoism is a very old Chine se religion which advanced around 500 BC (Personal Interview, 2009). Exact details of Shintoisms origins is very difficult to receive because of the fact that that there are no official texts or leaders within this movement. As a result, Shintoism is defined as a set of values and principles that developed in the larger framework of Japanese society (Personal Interview, 2009). This belief system has grown in conjunction with Buddhism. Actually, many scholars believe that in early Japanese history, both Shintoism and Buddhism could not be distinguished from each another.Even though Shintoism expanded from a Buddhism framework, it has been recognized as a separate religion and spiritual counseling of living. The fundamental element of Shintoism concerns deities or Kami, who are accountable for the construction of Japan and the expansion of a variety of tribes that reside in the region (Handbook of Todays Religions, 2009). In general, the Kami that populate in Shintoism are benevolen t gods that play a constructive role in the growth of humanity. Accordingly, Shintoism does not dwell on the framework of divine discourse as it pertains to day-to-day living. Instead, Shintoism centers on the growth of life that is lived in search of additional supercilious social standards (Personal Interview, 2009). In many situations, Shintoism uses a large amount of its basic principles from the Confucian tradition.Even though Shintoism is extremely interlaced with both Confucian and Buddhist ideologies, it has been noted that there are dissimilar components of the practices which undoubtedly distinguish them. For example, Shintoism believes that ancestors are extremely respected and even worshipped. Also, all people are thought of as Kamis child (Personal Interview, 2009). In addition, there are four assertions that are significant in Shintoism, and include elements of tradition, love, hygiene, and worship (Personal Interview, 2009). Shintoism was established through these va lues.All of components of Shintoism center on the growth and founding of an optimistic relationship between a person and his or her environment. Shintoism looks to smooth the progress of the progress of man as it pertains to nature in a harmonious association. This harmony has the potential to be come through through intense worship however, it can also be attained through ceremonial offerings of both money and food. A large amount of followers are occupied in the offer a meal movement, which is basically when a person skips a meal on a monthly primer coat and instead donates his or her money to their religious institution for worldwide liberation and analogous activity (Personal Interview, 2009).After evaluating the general attraction of Shintoism to an private disciple, it is an all-purpose way of life that authorizes that the follower to follow a life that is Godly in nature. Even though the term Shinto is not easy to convert into English, the dewy-eyed translations that have been accepted entail that the follower lives a life that follows the ways of the Gods. Because of this, Shintoism is a spiritual element that encompasses the day-to-day life of an individual follower. It supplies the foundation for the progression of action and requires that all followers collect on actions and ideologies that are proportionate with how the Gods would act in a comparable situation. Therefore, Shintoism is not necessary tempting to plunder in because of what it guarantees the follower in the afterlife instead, Shintoism is tempting to be part of because it gives its followers numerous methods to connect with God in multiple ways.When the fundamental structures of both Christianity and Shintoism are evaluated against one another, it seems, at least initially, that there are definitely more(prenominal) noteworthy variations between the two religions than there are similarities. For example, Christianity is based upon the learning and labors of Christ, as outlined in the New Testament. However, Shintoism in actuality has no real texts, or even a religious set of guidelines that are to be followed by its followers. In addition, Christianity in general focuses on devotion to God through living a meaningful life that is supported by the teachings of Christ. Shintoism, on the other hand, does not have a fundamental leader that has served as the foundation for the general growth and expansion of the religion (Shintoism, 2009). Actually, as alluded to above, Shintoism was founded on an extended practice of harmonizing spiritual values that have been sustained in the framework of other religions such as Confucianism and Buddhism.Even though there are obviously distinguishable variations between the two religions, there actually appears to be one prominent resemblance that really should be taken into account for when evaluating these two religions. In spite of of the texts, in regards to the principles and leaders that are both living or not living within the framework of the religion, both Christianity and Shintoism call for paving a pathway of populace that will at long last show the way for a better life. When it comes to Christianity, a person could successfully dispute that this religion primary deals with the teachings of Christ as an essential method of bringing a person closer to God. Christ guaranteed his followers that if they lived a life that pursued his teachings, they would, in turn, become closer to God and the Gods Kingdom. If a person closely examines the teachings of Christ as depicted in the New Testament, it is obvious that Christ desired for his followers to be in love with and take pleasure in all of humanity. This message is obvious, as Jesus promotes that followers feel affection for God and their neighbors in the same capacity.In regards to Shintoism, it is obvious that the conduit that followers are supposed to attribute to is one that also cultivates a conduit that will ultimately show the way to G od. Even though it seems as though Shintoism deals more with a persons connection with nature, the bond that is fashioned is comparable man needs to live in agreement withthe environment that is around him in order to strike an advanced existence and successfully come nearer to God. In Christianity, the corridor that a person is supposed to follow is essentially written in the scripture however, in Shintoism, the corridor that a person needs to follow is sustained through practice and admiration for the magnificence and majesty of nature. In both of the religions, however, the objective is to make certain that a person follows a corridor that ultimately brings them to God. This fundamental principle is one that is the foundation for the growth and foundation of both of these religions.Even though both Christianity and Shintoism primarily emphasize on following a conduit that will in due course lead to connecting with God, as time has progressed, Christianity seems to have taken on an unshared element that particularly separates it from the fundamental foundation of Shintoism. The principles of Shintoism, when properly implemented by the follower, become an essential component of every-day life. Shintoism is not a religious order that can be taken control of or divided from a person (Shintoism, 2009). As such, Shintoism has been distinguished to have a spiritual aspect that establishes it as a crucial element in the day-to-day life of a person. Even though Christianity seems to convey a comparable message-that a person needs to approach on a daily basis in the same way in which Christ would-the development of modern Christianity has gotten rid of the day-to-day impact of Christ on the individual person. Christianity seems to have become an observance that happens outside of the non-spiritual life of the person. A person attends church on a weekly basis in order to worship in Christs name. Even though Christ is considered to be an essential element of a perso ns life, this appropriation of the spiritual makes it very hard for the person to maintain Jesus as an encouraging element that encourages certain behaviors on a daily basis.Even though both Christianity and Shintoism present themselves as a tool for the spiritual progression of a person, the transformation of Christianity seems to have had an unconstructive effect on separating religion from the daily activities of a person. Notwithstanding, Christianity seems to have remained among the most known worldly religions. Consequently, even though some amount of transformation has taken place, Christianity still remains appealing to a majority of people.When the fundamental principles of both Christianity and Shintoism are look at in detail, the general petition of each of the religions seems to come from a more widespread plan of action for an individual. Under the principles of both Christianity and Shintoism, the individual follower is provided with a pathway to pursue. In most occas ions, this pathway gives the follower a way for them to live a godly existence that will ultimately bring them closer to Him. This important element is what makes both of the religions so interesting for their followers.

An overview of atrial fibrillation

An overview of atrial fibrillationSection1Atrial fibrillation (AF) is a condition when the message does not beat to its normal speeds or rhythm, often it beats express than it should. This irregularity leads to an change magnitude assay of stroke and remainder. The pump function of the heart deterio aims as a result of the un-coordination (due to uncoordinated excitation of muscles). The net result of damage pump action is the upper chambers of the heart contract randomly and at times too quick for the heart to relax before it contri simplye contract again legally.At the junction of the pulmonary veins in the left atrial musculature, subnormal impulses fire which override the heart natural pace maker.thither argon 3 major classifications for AFParoxysmal AF- lasts from 30 seconds to 7daysPersistent AF- longer the 7daysPermanent AF- AF that fails to terminate using cardioversion, or is terminated but relapses within 24hours.If in that location atomic number 18 no obvious c ause and all investigations ar normal, this is know as l unmatched AF. Lone AF tends to occur in Paroxysmal cases.Otherwise the nearly common causes beischaemic heart diseasehypertensionmitral stenosishyperthyroidismOther causes which arent as common are can be classified into 3 sub catagoriesCardiac Rheumatic heart disease, Sick sinus syndrome, Pre-excitation syndromes (such as Wolff-Parkinson-White syndrome) and heart failure. Less commonly, congenital heart disease, atrial myxoma , atrial septal defect, pericardial disease, and cardiomyopathy.Non-cardiac Drugs (e.g. bronchodilators/thyroxine), Electrolyte depletion infection, Pulmonary embolism, Lung cancer Diabetes.Lifestyle Obesity, high caffeine or alcohol intake1.A fast pulse (often 140bpm) which whitethorn or whitethorn not be irregular is the most common symptom of AF however it is likewise accompanied by tiredness, breathlessness, dizziness, angina1, syncope, reduced exercise tolerance, or polyuria2. The decreased mi ght of the pumping of the heart may result in the reduction of subscriber line pressure.AF is diagnosed by the use of an ECG and is characterised by the absence of consistent P waves and presence of fibrillation.The method of circumspection of suffers of AF has two main strategies, either by the control the arrhythmia aspect of the condition or by the tachycardia stance of the condition. Rhythm arbitrary drugs implicate flecainide (and other akin(predicate) drugs), beta-blockers ( finickyly sotalol), and amiodarone. Rate controlling drugs such as beta-blockers bisoprolol atenolol or the calcium channel blockers verapamil ordiltiazem.Thrombolytic and antiplatelet drugs are also employ to manage the thromboembolic risk. There are non pharmacological ways to manage AF, the most common being cardioversion.Aspirin inhibits cycloxygenase from producing thromboxane A2 which is responsible for platelet activation and therefore aggregationDiltiazem of use in AF for its affects on calcium channels on the heart. The blocking of calcium channels reduces excitability of cardiac muscle and thus decreasing fibrillations it also decreases the force of contractionAtenolol is a beta receptor blocker(a classII), it decreases the effects of the sympathetic drive to the heart, such that the neurotransmitters adrenaline and noradrenaline are competitively blocked. Thus the levels of camping area decrease. cAMP mediates many events in the heartdecreases stability in resting potencys (phase 4) of nodal tissue(AVN conduction SAN firing). In nodal tissue(myocytes) a decrease in cAMP reduces Ca2+ entry thus action electromotive forces take longer, it also causes repolarisation to longer i.e. increasing the refractory periodAmiodarone has all four classes of activity (of Vaughan Williams system subscribe to APPENDIX) however its main method of action is its class III mechanism. By the blocking potassium channels the potassium efflux in an action potential is blocked, thu s action potentials duration is a prolonged refractory period (causing a region of unidirectional block remain refractory for longer trenchantly having a bi directional block)3Verapamil a non selective calcium channel blocker (classIV), by reducing the Ca2+ into the cell through L-type channels in the nodal tissue (SAN AVN) depolarization takes longer as does the refractory period causing s starter AVN conduction. Reduces tachycardic impulse from AVN to the ventricles and also AVN re-entrant rhythms. Phase 2 is limited in nodal tissue (myocytes and purkinje fibres) reduces triggered automaticity4.Warfarin inhibits the effective synthesis of biologically active forms of the vitamin K-dependent clotting factors II, VII, IX and X, as well as some regulatory proteins.Flecainide a class1c sodium channel blocker.There is decreased diastolic excitability and Phase 0 (depolarization) takes longer as does the refractory period together causing slower conductions4.Propafenone is a class1c so dium channel blocker.There is decreased diastolic excitability and Phase 0 (depolarization) takes longer as does the refractory period together causing slower conductions4.digoxin is a K+/Na+ ATPase inhibitor which leads to an increase in the intracellular concentration of sodium this stimulates of sodium-calcium exchange as a result there is an increase in the intracellular concentration of calcium causing stronger less frequent contractions.Cardioversion may be tried in some hoi polloi with AF. The heart is given a controlled electric shock to try to restore a normal rhythm1.Catheter ablation is a procedure that very dispensefully destroysthe diseased area of your heart and interrupts abnormal electrical circuits. It is an option if medicinal drug has not been effective or tolerated1.A pacemaker may be fitted alternatively to drug treatment when it is not fascinate of failing1.Section 2AF is the most common rhytm disorder of the heart with up to 500,000 sufferes in the UK1. In the UK over 46,000new cases of AF are diagnosed each year5. The incidences increase with age, with a high incidence in men, when data is adjusted for age6. AF is uncommon in the young unless there is an existing heart disorder. At 50-59years of age, the prevalence is around 0.5%. At 80-89years of age, the prevalence is around 9%.Section 3AF is a significantly increases the chance of stroke and emboli. The decision to use antithrombotic therapy involves a complex balancing of risks, benefits, and costs. The probabilities of stroke, discharge complications, and death the associated costs of all treatment options and outcomes and the quality of life associated with treatment and disability. These oblige shown that warfarin therapy is generally cost-effective and often cost-saving. However, the economic value of antithrombotic therapy in toll of cost-effectiveness is most strongly influenced by 2 factors stroke risk and perceived quality of life.The cost-effectiveness models indic ate that warfarin can be cost-effective or, indeed, cost-saving for a tolerant variety of patients with AF, provided that it is prescribed appropriately based upon stroke risks7In patients at high risk of stroke, anticoagulation is most cost effective, but not for those at low risk of stroke8.Aspirin 75mgx28 1.66, Aspirin 300mgx28 0.55, Warfarin 1mgx28 1.10, Warfarin 3mgx28 1.15, Warfarin 5mgx28 1.21, Atenolol 25mgx28 0.82, Diltiazem MR 60 mgx84 3.52, Diltiazem MR 60 mgx56 (or over 70yrs), verapamil 40mgx80 1.55.Section 4Symptoms should be monitored often AF has no symptoms, however you should look for the common presenting symptoms (stated in section 1).TestsHeart Rate- Should be done when treating with rate lowering drugsElectrocardiography- every 12monthsblood electrolytes, urea and creatinine- 1-2 weeks after initiation, and 1-2 weeks after reaching the maintenance dose, then every 6 months. For Beta-blockers, digoxin, amiodaroneMonitor blood pressureLiver function tests- every 6months for amiodaroneThyroid function test- when using amiodaroneeye examinations- annual eye examinations.Plasma levels- for digoxin, shortly after initiation or after a dose increaee. 0.7and 2.0nanograms per millilitreDrugs to reduce the risk of thromboembolism (warfarin, aspirin and clopidogrel)The target INR for oral anti coagulants is 2-3 usually 2.5. Patients should be considered for warfarin use if risk is perceived to be medium or high according to straitlaced (see appendix)9. It is important that INR be measured chance(a) or alternate days at initiation of treatment. past at longer intervals depending on dose response up to 12 weeks10. Note the importance of increased monitoring as drugs are added to the regimen, pre-adjustment to warfrin are sometimes necessary e.g. decreasing dose by one or two thirds before initiation of amiodarone1.Section 5Although systematic reviews have shown that aspirin reduces the rate of stroke by 25%8 The Atrial Fibrillation, Aspirin Antico agulation Study demonstrated a reduction of strokes by 64% per year with warfarin (INR 2.8-4.2), compared with placebo, a 3.5% per year reduction. A non-significant reduction in stroke was seen with aspirin 75mg8. Where warfarin is contraindicated or patient requests not to initiate therapy, it has been assemble that a combination of antiplatelets (aspirin and clopidogrel) was associated with a significant reduction in major vascular events compared with aspirin alone. The number of large number that would need to be treated with aspirin plus clopidogrel for 3.6years to prevent one vascular event was 421.According to a meta-analysis the combination of both aspirin and warfrin yielded no significant reduction in stroke rates and had increased side effects8.No mortality difference was nominate between rhythm control and rate control. Although for people older than 65years of age or those with coronary artery disease, a significant difference was found in favour of rate control in t erms of all-cause mortality. Studies showed significantly higher rates of hospitalisation and adverse events in the rhythm control group and no difference in quality of life between the two groupsa.Incidence of ischaemic stroke, bleeding and systemic embolism was similar in the two groups, but certain malignant dysrhythmias were significantly more likely to occur in the rhythm control groupa. No cognitive make up was seen with the use of rhythm controlling drugs. Quality of life scores were similar in both groups. Therefore it is recommended that rate control, is used as it is less costly11.IA, IC and III drugs are effective in maintaining sinus rhythm but increased adverse effects. Class IA drugs may increase mortality.Calcium antagonists versus digoxin seven-spot studies found no difference in average heart rate between calcium antagonists verapamil or diltiazem and digoxin either at rest or during periods of normal daily activity. Studies have found calcium antagonists resulted in a lower heart rate during exercise, compared with digoxin2.Beta-blockers versus digoxinThree studies found no difference in average heart rate between digoxin and beta blockers while at rest or during periods of normal daily activity. However, the beta blockers atenolol and labetalol controlled heart rate during exercise more effectively than digoxin did2.Beta-blockers versus calcium antagonistsOne crossover study found no difference between the calcium antagonist diltiazem and the beta-blocker atenolol in terms of either the mean heart rate over 24 hours or during exercise2.Beta-blockers with digoxin versus beta-blockersOne crossover study found no statistically significant differences in heart rate during periods of exercise. Some studies found the beta-blocker atenolol used in combination with digoxin to be associated with a lower heart rate over 24 hours than atenolol alone2.Calcium antagonists with digoxin versus calcium antagonists quadruple crossover studies found that cal cium antagonists diltiazem or verapamil used in combination with Digoxin to be more effective in controlling heart rate over 24 hours, as well as during periods of exercise, than either diltiazem or verapamil alone2.Section 6Many people whom suffer from AF suffer no symptoms, some have been diagnosed incidentally1. It is in these patients that concordance is a particular issue. Education as to the risks and complications of the condition are necessary to win optimum concordance. It is important that patients are aware the side effects (SE) as well as the dosage regimen. Many of the dugs used in the management of AF have common and serious side effects which patients should be trained to spot.Interactions and side effects of note. Further information can be derived from the British National formulary (BNF) and a comprehensive analysis available in the most current Stockleys drug interaction. Classes of drugs have been mentioned although this does not mean that the entire class will interactAmiodarone Interactions Anti-arrhythmic (rate and rhythm modulating), Antibiotics, Anti coagulants, Tricyclic antidepressants, mizolastine, thyroid hormones, diuretics and phenytoin10.it is of note that due to its long half life amiodarone may still interact some(prenominal) months after treatment is stopped particularly relevant in the switching over of treatments.Amiodarone reduces the clearance of warfarin, prolonging prothrombin times (PTs) and elevating international normalized ratios (INRs). To avoid bleeding complications, the patient being put on amiodarone must have their current dosage of warfarin reduced by at least terzetto and PT and INR closely monitored until they are stabilized15. Although routine eye examinations should occur to asses the ocular effects of amiodarone, if a patient experiences any visual impairment the treatment should be stopped10. Patients should be aware for the signs of thyroid dysfunction (signs and symptoms of which included in appen dix 1)Warfarin interactions Alcohol, amiodarone, propafenone, analgesics, antibiotics, antidepressants, antiepileptics, thyroid hormones, ulcer healing drugs, lipid regulating drugs, hormones, corticosteroidsWarfarin levels are easily effected by changes in diet, major changes in diet should be done in consultation with healthcare professional, commonly eaten foods that are known to interact with warfarin are cranberry, grapefruit and vitamin K rich foods16. bleed or bruise easily. Also, if you bleed, the bleeding may not stop as readily as normally. For example, you may have bleeding gums nosebleeds prolonged bleeding from cuts blood in the urine.Beta blocker interactions Antiarrhythmics (rhythm and rate modulating), antibiotics, antidepressants, mizolastine, antipsychotics and diuretics.Beta blockers should be avoided in people with asthma, or with chronic obstructive pulmonary disease13, Beta-blockers should not be stopped suddenly unless absolutely necessary there is a risk of rebound in the condition13. Doses are titrated for patients and are gradually increased10.Digoxin interactions Antiarrhythmics (rate and rhythm modulating), diuretics, anti biotics and anti epileptics.Signs and symptoms of digoxin toxicity are important to report promptly. Digoxin toxicity may cause drowsy, dizzy, and affect your vision, disorientation, confusion, headach or disyurbed vision14.Flecainde interactions Antiarrhythmics (rate and rhythm modulating), antidepressants, antihistamines, antipsychotics, diuretics and tolterodineRoughly 1% of the general population and 10% of asthma suffers are allergic to aspirin12. Each drug has the potential for interaction with other medication and even food.Self help adviceIn order to minimise the risk of stroke and heart attacks it is important for patient to contract practical advise on diet as this will impact on blood cholesterol levels, weight management and blood pressure it is of particular importance when the patient is diabetic.I mportant components in a healthy diet are low fat and salt intakes, with an emphasis on complex carbohydrates found in vegetables. Advice on the sources of esstential fatty acids should be given (for example nuts and oily fish). Smoking cessation counseling and Nicotine replacement therapy should be offered, discussing the statistical signification smoking alone contributes to the Cardio vascular events.Section 7Pharmacists have contact at various stages along a patients treatment. A specialist PCT druggist may manage patients, prescribe, review and monitior. A community pharmacist should attempt medicine use reviews and prepare to make interventions on prescription(prenominal)s when appropriate. Clinical pharmacists are relate in monitoring and providing guidance on protocols and current evidence.In the future there will be an increased scope for pharmacists to play a big role when full patient records become available, full clinical reviews may be conducted taking into accoun t the persons history (familial, drug, treatment, condition) and make appropriate interventions and recommendations according to the most current evidence.Section 8In order for the condition and the services to run effectively is necessary to run audits regularly. This will ensure the national standards are met. Nice guideline audit criteriaAll people presenting to primary or secondary care with a hypertension, heart failure, diabetes made or stroke and observe to have an irregular pulse to be offered an ECG and any new diagnosis of AF recorded2.All AF patients in whom a rate-control or rhythm-control strategy is initiated to have their interest group in choosing a treatment strategy recorded2.All patients who are prescribed digoxin as initial monotherapy for rate control to have the reason for this prescription recorded where it is not obvious (e.g. sedentary patient presence of contraindication to alternative agents)2.All patients should be assessed for risk of stroke/thromboemb olism and given thromboprophylaxis according to the stroke risk and have this assessment and any antithrombotic therapy recorded2.It is important for pharmacists to keep uodate and maintaining a high levels of competenacy. Advice should be evidence based and current. There are regular updates produced by nice NICE and the Guidelines for atrial fibriliation are a good source of information.Section 9the National Service Framework for coronary heart disease has a chapter pertains to AF. Arrhythmias are of great importance Cardiac arrhythmia affects more than 700,000 people in England and is consistently in the top ten reasons for hospital admission, using up significant AE time and bed days. AFis the most common arrhythmia, affects up to 1% of the population (rising to 4% in the over 65s) and absorbs almost 1% of the entire calculate of the NHS to the NHS16. Of the three quality requirements there are two relevant in AF.Quality requirement one patient wear. People with arrhythmias re ceive timely and high-quality support and information, based on assessment of their needs16.Markers of good practicePeople with arrhythmias receive a formal assessment of their support needs and those at significantly increased risk of anxiety, depression or a poor quality of life receive appropriate care16.People with long-term conditions receive support in managing their indisposition from a named arrhythmia care co-ordinator16.Good quality, timely information about arrhythmic conditions is given by appropriately trained staff16.Quality requirement two diagnosis and treatment. People presenting with arrhythmias, in both emergency and elective settings, receive timely assessment by an appropriate clinician to ensure accurate diagnosis and effective treatment and rehabilitation16.Markers of Good Practice Initial TreatmentAll patients receive a hard copy of the ECG documenting their arrhythmia and a copy is position in their records.Patients who survive out-of-hospital cardiac arr est and patients presenting with pre-excited AF are assessed by a heart rhythm specialist prior to hospital discharge.The following patients are assessed urgently by a heart rhythm specialistPatients with syncope or any other symptom(s) suggestive of an arrhythmia and a personal history of morphologic heart disease or a family history of premature sudden deathPatients with recurrent syncope associated with palpitationsPatients with syncope and pre-excitationPatients with documented 3rd level AV block (not associated with acute MI)Patients with recurrent syncope in whom a life-threatening cause has not been excludedPatients with documented ventricular tachycardiaThe following patients are referred to a heart rhythm specialistPatients with a presumed diagnosis of ventricular tachycardiaPatients with Wolff-Parkinson-White (WPW) syndrome or asymptomatic pre-excitationPatients with symptomatic regular recurrent supraventricular tachycardia which is unsuccessfully treated with one type of medication or who would prefer not to take long-term medicationPatients with recurrent atrial flutterPatients with symptomatic AF despite optimal medical therapyFirst degree relatives of victims of sudden cardiac death who died below the age of 40 yearsPatients with recurrent unexplained fallsMarkers of Good Practice Ongoing TreatmentMechanisms are in place for urgent referral of patients with sustained or compromising arrhythmias for prioritisation of appropriate treatment.Implantable cardioverter defibrillators (ICDs) are considered in patients presenting with life-threatening ventricular arrhythmias and in those without demonstrable arrhythmia but identified as being at high risk.Catheter ablation is considered as the treatment of choice in patients presenting with sustained supraventricular tachycardia (SVT) other than AF, and cardioversion of recent onset AF is considered as early as is clinically safe.Where further hospital treatment is not recommended, a care plan is agre ed between the patient, GP and the arrhythmia care team, including follow up and support as required.Management of long term conditions and elderly also have a priority in the governments plans and frameworks for the future.Section 10Emphasis should be on patient centered care, projects such as near patient testing for warfarin have proved to be effective at managing patients and their potential complications.Primary care workers such as GPs PCT pharmacist should screen at risk patients. They shall be involved in the management of there condition frequently monitor patients. If required a referral can be made on lifestyle issues to manage the risk of stroke, e.g. if lipids are elevated may want to refer to a dietitian. Community pharmacists have a role in conduction medicines use reviews and be prepared to make inventions in prescribing, regimen concordance and side effect management/referral. It is of utmost importance that the specialist (cardiologist) makes clear recommendation and maintains communications with their counterparts in primary care.

Alzheimers Disease: Biology, Etiology and Solutions

Alzheimers Disease Biology, Etiology and SolutionsIntroductionAlzheimers disease (AD) is a type of dementia characterized by the progressive loss in cognitive function due to neurode constituentration that results in gradual memory loss and eventually the inability to carry out tasks of practiceaday living. The two types of AD be distinguished by age of onset and etiologies early-onset AD develops prior to age 65 and has strong genetic associations while late-onset AD develops after age 65 with a more complex etiology. Late-onset AD accounts for 90-95% of AD cases (Harman 2002). Aging is a strong risk factor for developing late-onset AD. given(p) that the global population of people ages 65 and up is expected to increase from 26.6 million in 2006 to 106.8 million by 2050 (Brookmeyer et al. 2007) AD is a growing popular health concern in regards to disease management and development of innovative treatments. The prevalence of AD globally is 4.4%, with 1 in 10 people all over age 65 and nearly one-third of people over age 85 affected by dementia in developed countries (Qiu et al. 2009). AD prevalence is the greatest in East Asia, fol pocket-sizeed by Western Europe, South Asia, and North America (Prince et al. 2015). Disease burden is anticipated to be the greatest in low and middle-income countries with the fastest growth in the elderly population and limited access to care (Prince et al. 2015). By 2050, the U.S. population of adults with AD is projected to increase to 13.2 million. With 43% of AD patients requiring a high level of care, the financial and healthcare burden of AD is expected to rise (Qiu et al. 2009). Given that the burden of AD will increase over the coming decades with costly impacts on health care and genial services, it is necessary to continue AD research to find a creator and develop raw therapies. EtiologyAlzheimers disease is a multifactorial disease with several genetic, person, and lifestyle risk factors that contri thate t o development of disease. Although many risk factors for AD seduce been identified a cause has not yet been found. Of the genetic risk factors identified, apolipoprotein E alleles, with ethnic and sex variability in risk of developing AD, and TREM2 gene transitions have the strongest associations with AD. Lifestyle risk factors include high blood pressure, obesity, diabetes, and education. The development of AD requires a combination of these risk factors that induce the production of neuro noxious amyloid beta (A) and neurofibrillary tangles (NFTs), the agents of AD. Apolipoprotein E (apoE) has been identified as playing a role in AD pathology. ApoE is naturally produced and is involved in lipid transport (Ridge et al. 2013 2018 Feb 27). In AD it is fancy that apoE regulation of A is altered (Kanekiyo et al. 2014). There are three apoE alleles that differ in the risk they confer to AD the 2 and 3 alleles are custodial but the 4 allele increases risk for AD (Ridge et al. 2013). Additionally, it appears that ethnicity modulates the risk of AD conferred by the apoE 4 allele, conferring greater risk among Caucasians and Japanese than Afri place Americans and Hispanics (Ridge et al., 2013). The apoE 4 allele is an established risk factor for the development of AD however it is not causative and the risk that carrying this gene confers is likely modulated by other factors such as ethnicity and lifestyle. Mutations in the TREM2 gene have also been affect in AD pathology. The TREM2 gene codes for a receptor expressed in myeloid cells, the genius innate insubordinate cell in the brain (Hickman and El Khoury 2014) and in greater abundance in the hippocampus and neocortex, brain structures affected by neurodegeneration in AD (Guerreiro et al. 2013 Jan 9). A rare missense mutation in the TREM2 gene was identified in Islanders that confers significant risk of AD (Jonsson et al. 2013 Jan 9) and a loss of function mutation increases the risk of late-onset AD in het erozygous carriers (Hickman and El Khoury 2014). This loss of function mutation promotes the production of A and numbers A phagocytosis and degradation (Hickman and El Khoury 2014). In admittance to the genetic risk factors discussed above, several lifestyle risk factors for AD have been identified including cardiovascular risk factors and obesity. Cardiovascular risk factors (smoking, hypertension, high cholesterol, and diabetes) in mid-life are associated with a 20-40% increased risk of AD in a dose-dependent fashion (Whitmer et al. 2005). Hypertension that develops in mid-life and persists into late-life is associated with a greater risk of dementia (McGrath et al. 2017). Furthermore, the risk of hypertension for AD in late-life might be influenced by sex, with females having a 65% increased risk of developing dementia if hypertensive in mid-life but no such association among males (Gilsanz et al. 2017). Midlife insulin resistance is also a risk factor for A accumulation (Ekbla d et al. 2018 Feb 23) and patients with diabetes and the apoE 4 allele have more A plaques and NFTs in the brain (Peila et al. 2002). Obesity is linked to AD via several single-nucleotide polymorphisms (Hinney et al. 2014). In people who are obese, leptin and adiponectin lose their neuro custodial role as the brain becomes resistant to leptin and the levels of adiponectin decrease (Letra et al. 2014). look into conducted by Nuzzo et al. (2015) further supports this association, finding that obese mice fed a high-fat diet had elevated A accumulation. Addressing these modifiable risk factors in mid-life may help reduce the risk of developing AD in late-life. Higher educational attainment and continued cognitive stimulation in later life are protective against AD. Amieva et al. (2014) found that individuals with AD who had education beyond 6 years of primary school showed delayed cognitive decline before diagnosis compared to individuals with less education. fighting(a) in cognitive leisure activities in late-life, like reading books, newspapers, and magazines, solving crossword puzzles, and attending courses and professional training, has a protective effect as salubrious (Sattler et al. 2012). Higher educational attainment may be associated with reduced risk of AD and delayed cognitive decline if AD develops because of its association with increased hippocampi and amygdaloid nucleuse size. In individuals with AD, the hippocampi are larger in those who had 20 years of cropal education compared to those with 6 years (Shpanskaya et al. 2014). The role of education in hippocampal size is further implicated by Tang, Varma, Miller, and Carlson (2017) who found that the left hippocampus is larger than the right, possibly due to education honing retrieval of verbal memory by the left hippocampus by means of increasing intellectual ability and literacy skills. BiologyAlzheimers disease results in the progressive loss of neurons in the cerebrum. The first structur es affected are the hippocampi followed by the amygdala (Pini et al. 2016). As the disease progresses so does neuronal loss throughout the cerebrum. In AD, A peptides and neurofibrillary tangles (NFTs) formed by tau protein cause synaptic damage that leads to apoptosis. Additionally, the innate immune system in the brain does not function properly in AD and therefore does not remove A peptides before they aggregate to form plaques. Amyloid beta is naturally produced in the brain by the cleavage of amyloid precursor protein (APP), but when APP is cleaved by -secretase A peptides are formed that can cause synaptic and mitochondrial damage and aggregate to form plaques (Querfurth and LaFerla 2010). In healthy individuals, A peptides are cleared by microglia and enzymes but these mechanisms deteriorate in individuals with AD and the A peptides accumulate and result in neurodegeneration (Sarlus and Heneka 2017). A plaques cause neuronal cell death by accumulating around neurons, impairin g normal function and inducing an unhealthy response. More attention late(a)ly has been given to A peptides, which lead to apoptosis in neurons through synaptic damage and inhibition of mitochondrial function. A peptides cause synaptic damage in the hippocampus by aggregating and creating pores in the cell membranes that allows calcium ion entry into the cell. Over time, these pores become non-selective and allow flux of large molecules like adenosine triphosphate and glucose that alters cell metabolism and disrupts homeostasis resulting in apoptosis (Seplveda et al. 2014). A also produces reactive oxygen species that initiate oxidative stress which leads to mitochondria in the cell releasing cytochrome C and inducing apoptosis (Querfurth and LaFerla 2010). Both A peptides and APP can enter the mitochondria where they disrupt the electron transport chain and ATP production (Caspersen et al. 2005 Reddy and Beal 2008). Synapses are sites of high mitochondrial operation because ATP i s needed for neurotransmitter release (Reddy and Beal 2008), so inhibition of mitochondrial activity by A also results in synaptic damage. NFTs are intracellular aggregations of hyperphosphorylated tau protein and also cause neurodegeneration. Tau protein is a component of the cytoskeleton of neural cells but when hyperphosphorylated tau proteins have an affinity for themselves and destabilize the cytoskeleton (Iqbal et al. 2005 Spillantini and Goedert 2013). Tau protein is phosphorylated by glycogen synthase kinase -3 (GSK-3) (Rankin et al. 2007) which can be activated by A peptides (Takashima 2006). Tau protein mediates synaptic damage by inhibiting extracellular signal-regulated kinase (ERK) signaling that is key in cell survival ( insolate et al. 2016). ApproachesCurrenttreatment of AD relies on two types of medications acetylcholine esteraseinhibitors (AChEIs) and N-methyl-D-aspartate (NMDA) receptor antagonists.AChEIs work by slowing the degradation of acetylcholine (ACh) by i nhibitingacetylcholine esterase which allows more ACh action at the synapses (Nelson and Tabet 2015).When cholinergic neurons are lost during the course of AD, ACh synthesis andreceptor signaling are reduced (Auld et al. 2002). AChEIs are mosteffective in slowing progression of cognitive decline in mild to moderate casesand less effective in severe AD (Gillette-Guyonnet et al. 2011).Memantine is an NMDA receptor antagonist (Tariot et al. 2004) that helps mitigate theloss of NMDA receptor function due to A peptides (Snyder et al. 2005). Memantine is noteffective for mild cases of AD (Nelson and Tabet 2015)but it is effective in moderate to severe cases, especially when used incombination with AChEIs (Tariot et al. 2004). AlthoughAChEIs and NMDA receptor antagonists are the current pharmacologicalal treatmentsavailable for AD, they are lone(prenominal) able to slow the progression of the disease andlose effectiveness as AD progresses. The challenge in designing a drug toprevent or cu re AD is the multifactorial nature of the disease with genetic andlifestyle risk factors. Even when non-pharmacologic interventions (controllingblood pressure, cognitive stimulation therapy, healthy diet and exercise, andmaintaining social networks) (Nelson and Tabet 2015)are used as part of a comprehensive treatment plan and initiated early indisease progression, the best that current treatments can cracking is to slow thenatural progression of the disease With ADprevalence expected to increase worldwide across all races and ethnicities, theculture of different populations is an important good will when designingintervention strategies. Social and economic barriers that prevent access tohealth care and social services among different populations need to beunderstood to identify and implement the best treatment specific to thatpopulation. Cultures also differ in how they view AD-related cognitive declineand may consider the memory loss a part of normal aging and therefore delaysee king treatment. An awareness of how cognitive decline in older age isdefined culturally, how cultures differ in caring for the elderly, and howbarriers to AD care services impacts each cultures choice of treatment is keyto developing successful interventions. Proposed SolutionsThe greatestchallenge in developing treatment for AD that can prevent AD development orprogression is that a specific cause has not yet been identified. However,recent research has identified new pharmacologic targets involved in theproduction of A and new therapies to reduce A and tau pathology. Research by Hu, Das, Hou, He, and Yan (2018)identified the -secretase BACE1 as a potential pharmacological target for thetreatment of AD. In a mouse model of AD in adults with BACE1 inhibition, it wasobserved that synaptic function change and A plaque governance was prevented.Although some clinical trials of BACE1 inhibitors have stalled, with Merckstopping its clinical trial of verubecestat in February 2018 (Merck 2018), there is still hope ofdeveloping pharmacologic treatments targeting A and tau proteins (Amgen 2017). A noveltherapeutic approach being researched is the use of optogenetic stimulation toreduce A and tau phosphorylation. Using a light flickering at 40 hertz, (Iaccarino et al. 2016)found they could stimulate brain waves called gamma oscillations in a mousemodel of AD and observed reduced A plaque formation and tau phosphorylation. Thismay lead to new non-invasive AD therapies, but more research is needed toinvestigate its effectiveness in humans. With treatmentapproaches that target the production of toxic A and abnormal tauphosphorylation, it is conceivable that in the future we may be better able toprevent and stop the progression of AD. ReferencesAmgen. 2017 Nov 2. Amgenand novartis announce expanded quislingism with banner alzheimers institutein pioneering prevention program. Amgen. accessed 2018 scotch 19.http//www.amgen.com/media/news-releases/2017/11/amgen-and-novartis -announce-expanded-collaboration-with-banner-alzheimers-institute-in-pioneering-prevention-program/.Amieva H, Mokri H, LeGoff M, Meillon C, Jacqmin-Gadda H, Foubert-Samier A, Orgogozo J-M, Stern Y,Dartigues J-F. 2014. Compensatory mechanisms in higher-educated subjects withAlzheimers disease a study of 20 years of cognitive decline. Brain13711671175. APOE gene. 2018 Feb 27.US Natl Libr Med. accessed 2018 Mar 5. https//ghr.nlm.nih.gov/gene/APOE.Auld DS, Kornecook TJ,Bastianetto S, Quirion R. 2002. Alzheimers disease and the basal forebraincholinergic system relations to -amyloid peptides, cognition, and treatmentstrategies. Prog Neurobiol. 68209245. Brookmeyer R, Johnson E,Ziegler-Graham K, Arrighi HM. 2007. Forecasting the global burden ofAlzheimers disease. Alzheimers Dement. J. Alzheimers Assoc. 3186191. Caspersen C, Wang N, YaoJ, Sosunov A, Chen X, Lustbader JW, Xu HW, Stern D, McKhann G, Yan SD. 2005.Mitochondrial Abeta a potential focal point for neuronal metabolic dysfunctioni n Alzheimers disease. FASEB J. 1920402041. Ekblad LL, Johansson J,Helin S, Viitanen M, Laine H, Puukka P, Jula A, Rinne JO. 2018 Feb 23. Midlifeinsulin resistance, APOE genotype, and late-life brain amyloid accumulation.Neurology10.1212/WNL.0000000000005214. Gillette-Guyonnet S,Andrieu S, Nourhashemi F, Gardette V, Coley N, Cantet C, Gauthier S, OussetP-J, Vellas B. 2011. Long-term progression of Alzheimers disease in patientsunder antidementia drugs. Alzheimers Dement J Alzheimers Assoc. 7579592. Gilsanz P, Mayeda ER,Glymour MM, Quesenberry CP, Mungas DM, DeCarli C, Dean A, Whitmer RA. 2017. egg-producing(prenominal) sex, early-onset hypertension, and risk of dementia. Neurology8918861893. Guerreiro R, Wojtas A,Bras J, Carrasquillo M, Rogaeva E, Majounie E, Cruchaga C, Sassi C, Kauwe JSK,Younkin S, et al. 2013. TREM2 variants in Alzheimers disease. N Engl J Med.368117-127Harman D. 2002.Alzheimers disease Role of aging in pathogenesis. Ann. N. Y. Acad. Sci.959384395. Hickman SE, El Khoury J.2014. TREM2 and the neuroimmunology of Alzheimers disease. Biochem Pharmacol.88495498. Hinney A, Albayrak O,Antel J, Volckmar A-L, Sims R, Chapman J, Harold D, Gerrish A, Heid IM, WinklerTW, et al. 2014. Genetic variation at the CELF1 (CUGBP, elav-like family member1 gene) locus is genome-wide associated with Alzheimers disease and obesity. Am J MedGenet B Neuropsychiatr Genet. 165B(4)283-93Hu X, Das B, Hou H, HeW, Yan R. 2018. BACE1 gash in the adult mouse reverses preformed amyloiddeposition and improves cognitive functions. J Exp Med. jem.20171831Iaccarino HF, Singer AC,Martorell AJ, Rudenko A, Gao F, Gillingham TZ, Mathys H, Seo J, Kritskiy O,Abdurrob F, et al. 2016. Gamma frequency entrainment attenuates amyloid loadand modifies microglia. Nature 540230. Iqbal K, del C. AlonsoA, Chen S, Chohan MO, El-Akkad E, bell C-X, Khatoon S, Li B, Liu F, Rahman A,et al. 2005. Tau pathology in Alzheimer disease and other tauopathies. BiochimBiophys Acta. 1739(2-3)198210. Jonsson T, Stefansson H,Steinberg S, Jonsdottir I, Jonsson PV, Snaedal J, Bjornsson S, Huttenlocher J,Levey AI, Lah JJ, et al. 2013. Variant of TREM2 associated with the risk ofAlzheimers disease. N Engl J Med. 368107-116Kanekiyo T, Xu H, Bu G.2014. ApoE and A in Alzheimers disease unintended encounters or partners?Neuron 81740754. Letra L, Santana I,Seia R. 2014. Obesity as a risk factor for Alzheimers disease the role ofadipocytokines. Metab Brain Dis. 29563568. McGrath ER, Beiser AS,DeCarli C, Plourde KL, Vasan RS, Greenberg SM, Seshadri S. 2017. contrast pressurefrom mid to late life and risk of incident dementia. Neurology8924472454. Merck. 2018 Feb 13.Merck announces discontinuation of APECS study evaluating verubecestat(MK-8931) for the treatment of people with prodromal Alzheimers disease.MERCK. accessed 2018 Mar 19.http//www.mrknewsroom.com/news-release/research-and-development-news/merck-announces-discontinuation-apecs-study-evaluating-ve.Nelson L, Tabet N. 2015.Slowing the prog ression of Alzheimers disease what works? Ageing Res. Rev.23193209. Nuzzo D, Picone P,Baldassano S, Caruana L, Messina E, Marino Gammazza A, Cappello F, Mul F, DiCarlo M. 2015. Insulin resistance as common molecular denominator linking obesityto Alzheimers disease. Curr Alzheimer Res. 12723735.Peila R, Rodriguez BL,Launer LJ. 2002. grapheme 2 diabetes, APOE gene, and the risk for dementia andrelated pathologies the Honolulu-Asia aging study. Diabetes. 5112561262. Pini L, Pievani M,Bocchetta M, Altomare D, Bosco P, Cavedo E, Galluzzi S, Marizzoni M, FrisoniGB. 2016. Brain atrophy in Alzheimers disease and aging. Ageing Res Rev.302548. Prince M, Wimo A, Guerchet M, Ali G-C, Wu Y-T, Prina M. 2015. World Alzheimer Report 2015 The global impact of dementia An analysis of prevalence, incidence, cost and trends. accessed 2018 March 18Qiu C, Kivipelto M, vonStrauss E. 2009. Epidemiology of Alzheimers disease occurrence, determinants,and strategies toward intervention. Dialogues Cli. Neuros ci. 11111128.Querfurth HW, LaFerlaFM. 2010. Alzheimers Disease. N Engl J Med. 362329344. Rankin CA, Sun Q,Gamblin TC. 2007. Tau phosphorylation by GSK-3 promotes tangle-like filamentmorphology. Mol Neurodegener. 212. Reddy PH, Beal MF. 2008.Amyloid beta, mitochondrial dysfunction and synaptic damage implications forcognitive decline in aging and Alzheimers disease. Trends Mol Med. 144553. Ridge PG, Ebbert MTW,Kauwe JSK. 2013. Genetics of Alzheimers disease. BioMed Res Int. 2013254-954.Sarlus H, Heneka MT.2017. Microglia in Alzheimers disease. J. Clin Invest. 12732403249. Sattler C, Toro P,Schnknecht P, Schrder. 2012. Cognitive activity, education and socioeconomicstatus as preventive factors for mild cognitive impairment and Alzheimersdisease. Psychiatry Res. 1969095.Seplveda FJ, Fierro H,Fernandez E, Castillo C, Peoples RW, Opazo C, Aguayo LG. 2014. Nature of theneurotoxic membrane actions of amyloid- on hippocampal neurons in Alzheimersdisease. Neurobiol Aging. 35472481. Shpanskay a KS, ChoudhuryKR, Hostage C, Murphy KR, Petrella JR, Doraiswamy PM. 2014. educationalattainment and hippocampal atrophy in the Alzheimers disease neuroimaging initiativecohort. J Neuroradiol. 41350357. Snyder EM, Nong Y,Almeida CG, Paul S, Moran T, Choi EY, Nairn AC, Salter MW, Lombroso PJ, GourasGK, et al. 2005. Regulation of NMDA receptor trafficking by amyloid-. NatNeurosci. 810511058. Spillantini MG, GoedertM. 2013. Tau pathology and neurodegeneration. gig Neurol. 12609622.Sun X-Y, Tuo Q-Z,Liuyang Z-Y, Xie A-J, Feng X-L, Yan X, Qiu M, Li S, Wang X-L, Cao F-Y, et al.2016. Extrasynaptic NMDA receptor-induced tau overexpression mediates neuronaldeath through suppressing survival signaling ERK phosphorylation. Cell DeathDis. 7(11)e2449. Takashima A. 2006. GSK-3is essential in the pathogenesis of Alzheimers disease. J Alzheimers Dis. 9309317.Tang X, Varma VR, MillerMI, Carlson MC. 2017. Education is associated with sub-regions of thehippocampus and the amygdala vulnerable to neurop athologies of Alzheimersdisease. Brain Struct Funct. 22214691479. Tariot PN, Farlow MR,Grossberg GT, Graham SM, McDonald S, Gergel I. 2004. Memantine treatment inpatients with moderate to severe Alzheimer disease already receiving donepezila randomized controlled trial. JAMA. 291317324. Whitmer RA, Sidney S,Selby J, Johnston SC, Yaffe K. 2005. Midlife cardiovascular risk factors andrisk of dementia in late life. Neurology. 64277281.

What Contribution Does Curleys Wife Make to Of Mice and Men? Essay

What Contribution Does Curleys Wife Make to Of Mice and Men?Curleys wife is the closely dangerous character in the novel, becauseshe is the loneliest one. Because of her need for attention, shedestroys George and Lennies dream of living off the fatta the lan.The appearance and clothing of Curleys wife have a symbolic meaning.She is described as a purty woman because she is always made up.Even on the ranch she has full, rouged lips and her hair lies inlittle rolled clusters, like sausages. Also her garments areseductive. When she speaks with George and Lennie, she wears a reddress and has red lips. The symbolic meaning of the colour red inliterature is danger. So Steinbeck foreshadows that she will bedangerous. She wears the said(prenominal) dress in the bunkhouse, as when shespeaks with Lennie at the end of the novel. The reader senses thatsomething bad will happen the death of Curleys wife.Curleys wife does not have a best life on the ranch. The relationshipbetween her and Curle y is miserable. She hates her husband and isreally glad when Lenni...

Yin and Yang: the Nature of Scientific Explanation in a Culture Essays

Yin and Yang the Nature of Scientific Explanation in a CultureABSTRACT I explore the nature of scientific explanation in a culture centering on the doctrine of yin and yang combine with that of v phrases, wu-hsing (YYFP). I note how YYFP functions as an alternative to the causal vogue of thinking, as well as the meaning of scientific explanation in a culture. I also consider whether a scientific conception becomes metaphorical when it is superseded by an alternative organizing concept. To a Western eye, or even to a contemporary Eastern eye, many explanations given under the doctrine of yin and yang combined with that of five phases (wu-hsing), apparently intended to be scientific, would seem either absurd or too arbitrary at first sight. An intriguing fact, however, is that the doctrine of yin and yang and that of five phases (hereafter YYFP) has prevailed until quite recently in almost all the areas of Far-Eastern cultures including medicine, astronomy, music, dance, architec ture, geomancy.In this essay, I pay attention to the questions such as how YYFP functioned as an alternative to the causal course of thinking, and what it is to be a scientific or theoretical explanation in a culture. I also consider the question of whether a scientific concept becomes metaphorical when it is superseded by an alternative organizing concept. Let me begin with the development of the concept of YYFP, as you may not know in the first place what YYFP is.Until close to the 4th century B.C., yin and yang were current words for sunshine and shade and were used separately from the five phases of change. Soon after, they came to be included in the six khi (six powers or forces) of Heaven. The six chi refer to wind, rain, dark, light,... .... Recent developments in quantum physics, biology and information science have put us in a plant where we question the uniqueness of the causal-mechanical model of science. But these developments, even though sciences based on non-caus al concepts might dominate in the culture, would not eradicate the causal way people have viewed the world and themselves, but only relegate the concept of spend a penny to the realm of metaphor, a rhetorical way of putting things. The concept of cause then would no longer be a scientific concept, but would still be alive in the culture. What brings a change in the commonplace worldview then? This would be the question I still have to ask. Notes(1) Tr.(in Korean)& ed. by Chung Young Ho (Jayou-Moongo, 1993), pp.22-23. English translation is mine.(2) Cf. Tung Chung-suh, Chun-chiu fan-lu (Luxurian Gems of the Spring and spill Annals).