Nearly 5 million Americans have heart failure today, with an incidence approaching 10 per 1000 population among persons older than 65 years of age. Heart failure is the reason for at least 20 percent of all hospital admissions among persons older than 65. Over the past decade, the rate of hospitalizations for heart failure has increased by 159 percent. 2 In 1997, an estimated $5,501 was spent for every hospital-discharge diagnosis of heart failure, and another $1,742 per month was required to care for each patient after discharge. Accordingly, substantial efforts have been made to identify and treat the factors that predict recurrent hospitalization. End points of large randomized trials now include the effect of the studied intervention on the rate of hospital admissions. For example, angiotensin-converting–enzyme (ACE) inhibitors, angiotensin-receptor antagonists, beta-blockers, spironolactone, biventricular pacing, coronary bypass surgery, and the use of multidisciplinary teams to treat heart failure have all been shown to reduce the rate of hospitalizations substantially, as well as to reduce mortality or improve functional status. 3-5 Considerable debate has focused on the mechanisms that reduce the rate of admissions and on the type of physician who should care for patients with heart failure. In the United States, more than two thirds of patients with heart failure are cared for exclusively by primary care practitioners. Multiple clinical trials completed during the past 15 years have unequivocally shown a substantial reduction in mortality for patients with systolic heart failure. Simultaneously, however, large epidemiologic surveys, such as the ongoing Framingham Study, have not documented any meaningful change in overall death rates. (Death seems to have been delayed, however, and occurs a longer time after major cardiac events such as a myocardial infarction.) Symptomatic heart failure continues to confer a worse prognosis than the majority of cancers in this country, with one-year mortality of approximately 45 percent. 6,7 Why have the newer and successful therapies failed to result in a meaningful reduction in mortality due to heart failure? It is important to recognize that heart failure is a clinical syndrome arising from diverse causes. Not all patients with the condition have poorly contracting ventricles and a low ejection fraction. Many have uncorrected valvular disease, such as aortic stenosis or mitral regurgitation, or abnormal filling, resulting in diastolic heart failure. A large majority of patients with heart failure are elderly, and 75 percent of patients have a history of hypertension. Many patients have at least one serious coexisting condition, in addition to advanced age. Such patients have not usually been subjects in investigational trials. Moreover, until recently, the majority of patients entered into trials of investigational drugs were middle-aged white men with heart failure due to ischemic cardiomyopathy. Fewer women and members of racial minorities have taken part in trials, and very few trials have included persons older than 75 years of age. Thus, despite the acknowledgedsuccesses of the therapies outlined below, there is much to be done in the prevention and management of heart failure in the large subgroups of patients who are not well represented in trials. Certainly, successful treatments have not been systematically applied to the majority of patients with heart failure, and for the reasons stated above, those that have been applied may not be efficacious. Although heart failure is a major public health problem, there are no national screening efforts to detect the disease at its earlier stages, as there are for breast and prostate cancer or even osteoporosis. Heart failure is largely preventable, primarily through the control of blood pressure and other vascular risk factors. Yet, until recently, the factors that render a patient at high risk for heart failure had not been clearly defined or publicized. The guidelines for the evaluation and management of chronic heart failure that were published recently by the American College of Cardiology and the American Heart Association have corrected this deficit. 8 The writing committee developed a new approach to the classification of heart failure that emphasizes its evolution and progression and defined four stages of heart failure. Patients with stage A heart failure are at high risk for the development of heart failure but have no apparent structural abnormality of the heart. Patients with stage B heart failure have a structural abnormality of the heart but have never had symptoms of heart failure. Patients with stage C heart failure have a structural abnormality of the heart and current or previous symptoms of heart failure. Patients with stage D heart failure have endstage symptoms of heart failure that are refractory to standard treatment. This staged classification underscores the fact that established risk factors and structural abnormalities are necessary for the development of heart failure, recognizes its progressive nature, and superimposes treatment strategies on the fundamentals of preventive efforts. The classification is a departure from the traditional New York Heart Association (NYHA) classification, which has primarily been used as shorthand to describe functional limitations. 9 Heart failure may progress from stage A to stage D in a given patient but cannot follow the path in reverse. In contrast, a patient with NYHA class IV symptoms might have quick improvement to class III with diuretic therapy alone. This staged heartfailure classification promotes a way of thinking about heart failure that is similar to our way of thinking about cancer — that is, the identification and screening of patients who are at risk, patients with in situ disease, and patients with established or widespread disease. The ensuing discussion about the treatment of heart failure is keyed toward this new staging classification.

the syndrome of heart failure

The traditional view that heart failure is a constellation of signs and symptoms caused by inadequate

performance of the heart focuses on only one aspect of the pathophysiology involved in the syndrome. Currently, a complex blend of structural, functional, and biologic alterations are evoked to account for the progressive nature of heart failure and to explain the efficacy or failure of therapies used in clinical trials. 10 For example, the rationale for the use of betablockers in a patient with a poorly contracting heart is based on a conceptual framework broader than that which suggests the treatment of congestion with diuretics or digoxin. The rationale for using beta-blockers is predicated on an understanding of the role of the sympathetic nervous system in promoting the release of renin and other vasoactive substances that trigger vasoconstriction, tachycardia, and changes in myocytes that lead to disadvantageous ventricular dilatation. Indeed, recent reviews have combined several models that had been used previously to understand heart failure in order to illustrate more fully the cascade of mechanisms, as well as the opportunities for intervention. 11 Thus, the hemodynamic model of heart failure emphasized the effect of an altered load on the failing ventricle and ushered in the era of vasodilators and inotropic agents. The neurohumoral model recognized the importance of activation of the renin–angiotensin–aldosterone axis and the sympathetic nervous system in the progression of cardiac dysfunction. More recently, efforts to antagonize the effects of circulating norepinephrine and angiotensin II have shifted with the recognition that these and other vasoactive substances are also synthesized within the myocardium and therefore act in an autocrine and paracrine manner, in addition to their actions in the circulation. For example, brain natriuretic peptide is produced by the ventricular myocardium in response to stretch; its vasodilatory and natriuretic effects counteract the opposing actions of angiotensin II and aldosterone. Other studies have scrutinized myocytes from failing hearts in an attempt to detect abnormal signaling, gene expression, or contractile protein structure. Table 1 details many of the factors that contribute to the heart-failure syndrome as it is currently understood. Because no single pathophysiological model can account for the host of clinical expressions of heart failure, current therapy often targets more than one organ system, as outlined in Figure 1. Additional pathophysiological concepts that have become clinically meaningful areas for investigation or treatment are described below.

remodeling

Increased levels of circulating neurohormones are only part of the response seen after an initial insult to the myocardium. Left ventricular remodeling is the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function. Remodeling occurs in several

clinical conditions, including myocardial infarction, cardiomyopathy, hypertension, and valvular heart

disease; its hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis. 12,13

For example, after a myocardial infarction, the acute loss of myocardial cells results in abnormal loading conditions that involve not only the border zone of the infarction, but also remote myocardium. These abnormal loading conditions induce dilatation and change the shape of the ventricle, rendering it more spherical, as well as causing hypertrophy. Remodeling continues for months after the initial insult, and the eventual change in the shape of the ventricle becomes deleterious to the overall function of the heart as a pump (Fig. 2A). 14 In cardiomyopathy, the process of progressive ventricular dilatation or hypertrophy occurs without the initial apparent myocardial injury observed after myocardial infarction (Fig. 2B). Several trials involving patients who were studied after a myocardial infarction or who had dilated cardiomyopathy found a benefit from ACE inhibitors, beta-adrenergic antagonists, or cardiac resynchronization. 15-18 Such beneficial effects were associated with so-called reverse remodeling, in which the therapy promoted a return to a more normal ventricular size and shape. 15-18 The reverse-remodeling process is a mechanism through which a variety of treatments palliate the heart-failure syndrome.

mitral regurgitation

Another potential deleterious outcome of remodeling is the development of mitral regurgitation. As the left ventricle dilates and the heart assumes a more globular shape, the geometric relation between

the papillary muscles and the mitral leaflets changes, causing restricted opening and increased tethering of the leaflets and distortion of the mitral apparatus. Dilatation of the annulus occurs as a result of increasing left ventricular or atrial size or as a result of regional abnormalities caused by myocardial infarction. 19-21 The presence of mitral regurgitation results in an increasing volume overload on the overburdened left ventricle that further contributes to remodeling, the progression of disease, and symptoms. Correction of mitral regurgitation has been an appropriate focus of therapy.

arrhythmias and bundle-branch block

The myocardial conduction system is vulnerable to the same pathophysiological processes that occur in the myocytes and interstitium, with altered conduction properties observed in response to ischemia,

inflammation, fibrosis, and aging. Supraventricular arrhythmias, particularly atrial fibrillation, are often the precipitating events that herald the onset of either systolic or diastolic heart failure. 22 Elevated ventricular end-diastolic pressure in a patient with hypertension or abnormal myocardial function leads to atrial stretch, which in turn incites electrical instability. Recognition of the presence of atrial fibrillation in a patient is critical, since several studies have now demonstrated the effectiveness of oral anticoagulant therapy for the prevention of stroke. 23 Abnormal myocardial conduction can also lead to delays in ventricular conduction and bundlebranch block. Left bundle-branch block is a significant predictor of sudden death and a common finding in patients with myocardial failure. 24-26 Its presence also affects the mechanical events of the cardiac cycle by causing abnormal ventricular activation and contraction, ventricular dyssynchrony, delayed opening and closure of the mitral and aortic valves, and abnormal diastolic function. Hemodynamic sequelae include a reduced ejection fraction, decreased cardiac output and arterial pressure, paradoxical septal motion, increased left ventricular volume, and mitral regurgitation. 27-30 Ventricular arrhythmias are thought to be secondary to a dispersion of normal conduction through nonhomogeneous myocardial tissue, which promotes repetitive ventricular arrhythmias. The rate of sudden cardiac death among persons with heart failure is six to nine times that seen in the general population. 31 Major innovations in medical and device-based therapy for the primary and secondary prevention of lethal ventricular arrhythmias have occurred during the past decade but are beyond the scope of this article. Increasing use of implantable cardioverter–defibrillators has unequivocally reduced mortality in a subgroup of patients with heart failure.

diastolic heart failure

It is estimated that 20 to 50 percent of patients with heart failure have preserved systolic function or a

normal left ventricular ejection fraction. Although such hearts contract normally, relaxation (diastole)

is abnormal. Cardiac output, especially during exercise, is limited by the abnormal filling characteristics of the ventricles. For a given ventricular volume, ventricular pressures are elevated, leading to pulmonary congestion, dyspnea, and edema identical to those seen in patients with a dilated, poorly contracting heart. 32-35 Characteristics of patients with systolic heart failure and those with diastolic heart failure are compared in Table 2. Patients with diastolic heart failure are typically elderly, often female, and usually obese and frequently have hypertension and diabetes. Mortality among these patients may be as high as that among patients with systolic heart failure, and the rates of hospitalization in the two groups are equal. 36 The diagnosis of diastolic heart failure is usually made by a clinician who recognizes the typical signs and symptoms of heart failure and who is not deterred by the finding of normal systolic function (i.e., a normal ejection fraction) on echocardiography. Echocardiography may be useful in the detection of diastolic filling abnormalities. Unfortunately, unlike heart failure due to systolic dysfunction, diastolic heart failure has been studied in few clinical trials, so there is little evidence to guide the care of patients with this condition. Physiological principles used in the treatment of such patients include the control of blood pressure, heart rate, myocardial ischemia, and blood volume.

clinical assessment

Breathlessness, fatigue, and even edema may be due to a host of noncardiac conditions and do not necessarily indicate the presence of heart failure. Nevertheless, the clinician must have a high index of suspicion that the source of a patient’s problems may be cardiac and must become adept at assessing patients for fluid overload and cardiac abnormalities. Measurement of serum brain natriuretic peptide may aid in the diagnosis of heart failure. 37 Serial measurements of weight at office visits, combined with instructions for daily weighing at home, help to alert the clinician and the patient to the possibility of fluid retention. The patient should be evaluated regularly in an appropriate position (45-degree elevation), with notation of the jugular venous pressure. Hepatojugular reflux, presence of a gallop rhythm, and peripheral edema are key findings on physical examination that may indicate a need for additional diuretic therapy and may be prognostically important. 38

treatment of patients with stage a heart failure

Control of risk factors in stage A (e.g., hypertension, coronary artery disease, and diabetes mellitus) has a favorable effect on the incidence of later cardiovascular events (Fig. 3). Results from trials have shown that the effective treatment of hypertension decreases the occurrence of left ventricular hypertrophy and cardiovascular mortality, as well as reducing the incidence of heart failure by 30 to 50 percent. 39,40 Guidelines have recommended that the target for diastolic blood pressure in patients considered to be at high risk, particularly those with diabetes, be below 80 mm Hg, with the goal of further reducing morbidity and mortality. 41 Patients with diabetes have a high incidence of heart disease, with multiple adaptive and maladaptive biochemical and functional cardiac abnormalities. 42 ACE-inhibitor treatment of asymptomatic high-risk patients with diabetes or vascular disease and no history of heart failure has yielded significant reductions in the rates of death, myocardial infarction, and stroke. 43-45 The use of the angiotensin-receptor blocker losartan has been shown to delay the first hospitalization for heart failure in patients with diabetes mellitus and nephropathy. 46 In short, the goal of treatment in stage A is to prevent remodeling.

treatment of stage b, c, or d heart failure with or without symptoms

The goals of therapy for patients with heart failure and a low ejection fraction are to improve survival,

slow the progression of disease, alleviate symptoms, and minimize risk factors. Modifications of lifestyle can be helpful in controlling the symptoms of heart failure. For example, basic habits of moderate sodium restriction, weight monitoring, and adherence to medication schedules may aid in avoiding fluid retention or alerting the patient to its presence. Moderation of alcohol intake is advised; avoidance of nonsteroidal antiinflammatory drugs (NSAIDs) is also important. 47 NSAIDs have been associated with an increase in the incidence of new heart failure, decompensated chronic heart failure, and hospitalizations for heart failure. For selected patients, a regularly scheduled exercise program may have beneficial effects on symptoms. 48,49 ACE inhibitors decrease the conversion of angiotensin I to angiotensin II, thereby minimizing the multiple pathophysiological effects of angiotensin II, and decrease the degradation of bradykinin. Bradykinin promotes vasodilatation in the vascular endothelium and causes natriuresis in the kidney. The beneficial effects of ACE inhibitors in heart failure and after a myocardial infarction include improvements in survival, the rate of hospitalization, symptoms, cardiac performance, neurohormonal levels, and reverse remodeling. 50-52 ACE inhibitors have not been unequivocally shown to reduce the incidence of sudden death. They are recommended for many patients with stage A heart failure and all patients with stage B, stage C, or stage D heart failure. But unresolved issues persist. First, underuse of ACE inhibitors by physicians for fear of potential side effects has been a concern. Yet side effects are fairly predictable and reversible and can usually be successfully managed. Second, the optimal dose of an ACE inhibitor is uncertain. Most randomized trials have shown no difference in mortality between patients receiving high-dose ACE inhibitors and those receiving low-dose ACE inhibitors. 53-56 Finally, it is uncertain whether there are any meaningful differences among the many ACE inhibitors available today. Table 3 details some common clinical problems with recommended approaches. Beta-blockers have long been used for the treatment of hypertension, angina, and arrhythmias and for prophylaxis in patients who have had a myocardial infarction. This class of medication has had a remarkable effect on chronic heart failure. The primary action of beta-blockers is to counteract the harmful effects of the sympathetic nervous system that are activated during heart failure. The beneficial effects of these drugs have been demonstrated in trials involving patients with heart failure from various causes and of all stages. These effects include improvements in survival, morbidity, ejection fraction, remodeling, quality of life, the rate of hospitalization, and the incidence of sudden death. 3,57 Betablockers should be used in all patients in stable condition without substantial fluid retention and without recent exacerbations of heart failure requiring inotropic therapy. There are a few populations of patients in whom beta-blockers should not be used or should be used only with extreme caution. Such patients include those with reactive airway disease, those with diabetes in association with frequent episodes of hypoglycemia, and those with bradyarrhythmias or heart block who do not have a pacemaker. Although the short-term effects of beta-blockers may result in a temporary exacerbation of symptoms, their long-term effects are uniformly beneficial. Placebo-controlled trials involving long term treatment have shown improved systolic function after three months of treatment and reverse remodeling after four months. 18,58,59 In the United States, two beta-blockers are specifically approved for the treatment of heart failure: carvedilol and long-acting metoprolol. Currently, neither drug has proved to be consistently superior; both have shown significant clinical efficacy. Carvedilol is a nonselective b –adrenergic antagonist with alpha-blocking effects; metoprolol is a selective b 1 adrenergic antagonist with no alpha-blocking effects. A large trial comparing these drugs is nearing completion. However, the most frequently prescribed beta-blocker in the United States is atenolol; there have been no studies to date on the use of atenolol in patients with heart failure. Drugs that antagonize the sympathetic nervous system through alternative pathways, such as clonidine or moxonidine, have been less clinically useful in patients with heart failure. Available angiotensin receptor antagonists block the effects of angiotensin II at the angiotensin II subtype 1 receptor. The recently published guidelines recommend that these drugs should not be used as first-line therapy for heart failure of any stage but should be used only in patients who cannot tolerate ACE inhibitors because of severe cough or angioedema. 8 Several trials involving patients with heart failure have shown that angiotensinreceptor antagonists have efficacy similar to that of ACE inhibitors but are not superior. 60-62 On the other hand, in a randomized trial of patients with symptomatic left ventricular systolic dysfunction, the addition of valsartan to ACE-inhibitor treatment reduced the rate of the combined end point of death or cardiovascular events and improved clinical signs and symptoms of heart failure. 63 However, patients who were receiving beta-blockers, an ACE inhibitor, and the angiotensin-receptor blocker valsartan had more adverse events and increased mortality. More recently, the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was completed in patients with stage B heart failure — specifically, asymptomatic patients with hypertension and left ventricular hypertrophy on electrocardiography. Treatment with the angiotensin-receptor blocker losartan yielded improvements in cardiovascular morbidity and survival, as well as a decrease in the incidence of new-onset diabetes, as compared with treatment with the beta-blocker atenolol. 64 Thus, accumulating data lend support to the contention that angiotensin-receptor antagonists are a reasonable alternative to ACE inhibitors.

additional therapy for symptomatic patients with stage c or stage d heart failure

There is evidence to support the use of spironolactone, an aldosterone antagonist, in patients with advanced symptoms of heart failure — specifically, NYHA class III or IV symptoms. 65 In patients with advanced heart failure, circulating levels of aldosterone become elevated in response to stimulation by angiotensin II, and there is a decrease in the hepatic clearance of aldosterone due to hepatic congestion. Aldosterone stimulates the retention of salt, myocardial hypertrophy, and potassium excretion; spironolactone counteracts these responses. 66 The beneficial effects of spironolactone in heart failure may also include a decrease in collagen synthesis that promotes organ fibrosis. Since heart failure is a salt-avid syndrome resulting in intravascular volume overload, diuretics are a mainstay for controlling symptoms of congestion. Thiazide or loop diuretics are often prescribed, and combination therapy may be used to promote effective diuresis in advanced cases. 67,68 It is only within the past five years that a large, randomized, placebo-controlled study of digoxin for symptomatic patients with a low ejection frac- tion has been completed. There was no difference in mortality between patients receiving digoxin and patients receiving placebo, but there were decreases in the digoxin group in the rates of worsening heart failure and hospitalization. 69 Recent data suggest that the maintenance of a low serum digoxin concentration (<0.09 ng per milliliter) is as effective in reducing the rate of cardiovascular events as the maintenance of a higher concentration and is associated with a lower rate of toxic effects. 70 Elderly patients and those with renal insufficiency are more prone to toxic effects. There is a commonly observed and clinically important interaction between digoxin and amiodarone: digoxin levels can become markedly elevated after the introduction of amiodarone. There are some patients who cannot tolerate either ACE inhibitors or angiotensin-receptor blockers, usually because of hyperkalemia or renal insufficiency. In such patients who remain symptomatic despite diuretic and beta-blocker therapy, treatment with the vasodilator combination of hydralazine and isosorbide dinitrate may be an option. 71

nonpharmacologic therapy

Cardiac resynchronization therapy is an innovative, pacemaker-based approach to the treatment of patients with heart failure who have a wide QRS complex on 12-lead electrocardiography. The purpose of resynchronization is to provide electromechanical coordination and improved ventricular synchrony in symptomatic patients who have severe systolic dysfunction and clinically significant intraventricular conduction defects, particularly left bundle-branch block. A percutaneous, three-lead, biventricular pacemaker system is used; one lead is placed in the right atrium, one is placed in the right ventricle, and a third is passed through the right atrium, through the coronary sinus, and into a cardiac vein on the lateral wall of the left ventricle. This left ventricular lead constitutes the key difference between resynchronization therapy and standard dual-chamber pacing. Beneficial effects include reverse remodeling, resulting in decreased heart size and ventricular volumes, improved ejection fraction, and decreased mitral regurgitation. Clinical improvements in exercise tolerance, quality of life, and the rate of hospitalization have been documented. 72-78 To date, however, resynchronization therapy has not been shown to enhance survival.

revascularization and surgical therapy

Patients with heart failure of any stage who are at risk for coronary artery disease should be screened

for myocardial ischemia. Revascularization, through either a catheter-based or a surgical approach, often improves ischemic symptoms, improves cardiac performance, and reduces the risk of sudden

death. 79,80 Patients with stage C or stage D heart failure, who have heretofore been considered unacceptable candidates for surgery, may in fact derive substantial benefit from bypass surgery and additional techniques designed to reduce myocardial wall stress. Procedures to eliminate or exclude areas of infarction, repair mitral regurgitation, or support the failing myocardium are undergoing clinical trials. 81-83 Similarly, the role of mechanical devices that serve to support patients who are awaiting heart transplantation or are definitive therapy for endstage (stage D) heart failure continues to evolve, and such devices offer great hope to many patients who are not eligible for cardiac transplantation. 84 Many common clinical problems encountered in patients with heart failure remain unresolved. The role of anticoagulant therapy in patients with systolic dysfunction and sinus rhythm is unclear; neither the type of therapy needed nor the appropriate duration of treatment is known. There may be an important adverse interaction between aspirin and ACE inhibitors that will be clarified in upcoming trials. 85 The optimal care for patients with heart failure and preserved systolic function (diastolic heart failure) awaits further research. The value of revascularization in patients with symptoms of heart failure but without angina will be explored in an important trial that is slated to begin soon. 86 How will we identify patients with familial cardiomyopathy at an earlier stage? 87-89

How do we identify patients with the greatest risk of sudden death? What is the best way to prevent sudden death in a cost-effective manner? Who will be best served by mechanical cardiac-support devices? Can we afford optimal care for the growing number of patients with heart failure? These questions and many others will undoubtedly be answered in the years to come. Perhaps our most intensive investigations, however, should be reserved for efforts that have been shown to prevent this cardiac plague — the control of hypertension and vascular risk factors.

Namun, mesin era 1990-an belum dilengkapi komputer. Gejala overheat bisa dideteksi dengan munculnya gejala knocking saat berakselerasi.

* Langkah preventif
Periksa cooling system dan jumlah oli mesin secara berkala. Perhatikan indikator suhu mesin saat timbul knocking, dan segera tepikan mobil.

Kebocoran oli
Berkurangnya jumlah oli mesin secara drastis akan menyebabkan friksi pada komponen yang bergerak. Dampaknya,suhu mesin tinggi (overheat) dan keausan luar biasa. Penyebabnya adalah kerusakan pada baut penutup lubang pembuangan oli akibat terkena hantaman benda keras, atau kondisi sil-sil di mesin kurang bagus. Perlu juga cermati indikator oli di dasbor yang akan menyala bila kekurangan pelumas.

* Langkah preventif
Periksa oli secara berkala. Jangan menganggap remeh  indikator oli yang menyala. Itu menandakan bahwa pompa oli kehilangan tekanan.

“Water hammer”
Air tersedot ke ruang bakar akibat menerjang genangan air yang tinggi. Air yang jauh lebih padat dari udara, sampai memenuhi ruang bakar, tentu tidak dapat tekanan saat mesin bekerja pada langkah kompresi. Dalam kondisi katup tertutup, tekanan air akan menghancurkan komponen terlemah di ruang bakar, yakni piston.

* Langkah preventif
Ketahui ketinggian saluran masuk udara di mesin. Jangan sekali-sekali menstarter ketika mesin mati di tengah banjir. Buka busi, lalu start mesin untuk mengeluarkan air di ruang bakar.

“Timing belt”
Fungsinya sebagai penyelaras putaran kruk as dan katup sehingga keduanya tidak berbenturan. Namun, fatal akibatnya bila belt yang menghubungkan kedua mekanisme ini putus secara tiba-tiba. Kerusakan tak terelakkan lantaran piston akan menumbuk katup yang berada dalam posisi membuka.

Bila hal tersebut terjadi dalam putaran mesin tinggi, maka blok mesin bisa pecah. Kondisi ini bisa diminimalkan bila Anda tahu kerusakan yang terjadi. Mesin dengan perbandingan kompresi rendah atau yang dilengkapi turbocharger atau supercharger cenderung memiliki peluang lebih kecil terhadap kerusakan.

An unusually cool late spring may be helping keep the infection going in the U.S. Northeast, especially densely populated areas in New York and Massachusetts, the officials at the U.S. Centers for Disease Control and Prevention said.

And infections among healthcare workers suggest that people are showing up at work sick — meaning that workplace policies may be contributing to its spread, the CDC officials said.

The new strain of swine flu is officially a pandemic now, according to the World Health Organization.

So far the virus is causing mild to moderate disease, but it has killed at least 167 people and been confirmed in nearly 40,000 globally.

The United States has been hardest hit, with upward of 100,000 likely cases and probably far more, with 44 deaths and 1,600 hospitalized.

“The fact that we are seeing ongoing transmission now indicates that we are seeing something different,” the CDC’s Dr. Daniel Jernigan told a news briefing.

“And we believe that that may have to do with the complete lack of immunity to this particular virus among those that are most likely affected. And those are children,” Jernigan added.

“The areas of the country that are most affected, some of them have very high population densities, like Boston and New York. So that may be a contributor as well. Plus the temperature in that part of the country is cooler, and we know that influenza appears to like the cooler times of the year for making transmission for effective.”

Jernigan said in areas that are the most affected up to 7 percent of the population has influenza-like illness.

SUMMER OF FLU

“The United States will likely continue to see influenza activity through the summer, and at this point we’re anticipating that we will see the novel H1N1 continue with activity probably all the way into our flu season in the fall and winter. The amount of activity we expect to be low, and then pick up later.”

One worrying pattern: healthcare workers are being infected, and most reported they did little or nothing to protect themselves, the CDC’s Dr. Mike Bell said.

People coming into emergency departments or clinics need to be checked right away for flu symptoms and anyone working with such a patient needs to wear a mask, gloves and eyewear, Bell said.

“We’re beginning to see a pattern of healthcare personnel-to-healthcare personnel transmission in some of the clusters, which is also concerning, because it gets to the issue of people showing up to work sick,” Bell said.

Doctors, nurses and technicians who have flu can spread it to vulnerable patients, Bell noted.

As of May 13, the CDC said it had received 48 reports of healthcare workers infected with swine flu.

Detailed case reports on 26 showed that 13 were infected in a healthcare setting such as a clinic or hospital and 12 caught it from infected patients, the CDC said in its weekly report on death and disease.

What would surprise Pausanias—as it is surprising archaeologists—is how early that “beginning” actually may be. New pottery evidence from excavations by the Greek-American, interdisciplinary team of the Mt. Lykaion Excavation and Survey Project indicates that the ash altar—a cone of earth located atop the southern peak of Mt Lykaion where dedications were made in antiquity— was in use as early as 5,000 years ago—at least 1,000 years before the early Greeks began to worship the god Zeus.

In addition, a rock crystal seal, bearing an image of a bull, of probable Late Minoan times (1500-1400 BCE) and also found on the altar, suggests an intriguing early connection between the Minoan isle of Crete and Arcadia, and bears witness to another chapter in what now appears to be an especially long history of activity atop the mountain.

“Mt. Lykaion, Arcadia is known from ancient literature as one of the mythological birthplaces of Zeus, the other being on Crete,” noted Dr.Romano. David Gilman Romano is Senior Research Scientist at the University of Pennsylvania Museum of Archaeology and Anthropology and a co-director of the Mt. Lykaion Excavation and Survey Project.“

The fact that the ash altar to Zeus includes early material dating back to 3000 BCE suggests that the tradition of devotion to some divinity on that spot is very ancient. The altar is long standing and may in fact pre-date the introduction of Zeus in the Greek world. We don’t yet know how the altar was first used, and whether it was used in connection with natural phenomena such as wind, rain, light or earthquakes, possibly to worship some kind of divinity male or female or a personification representing forces of nature.” Below the altar in a mountain meadow is an ancient hippodrome, a stadium and buildings related to the ancient athletic festival that rivaled the neighboring sanctuary of Zeus at Olympia.

Although the Sanctuary of Zeus at Mt. Lykaion, just 22 miles from the extensively-studied Sanctuary of Zeus at Olympia, has been well known since antiquity, no excavations had taken place there in a century. The Mt. Lykaion Excavation and Survey Project, begun in 2004 with the first seasons of excavation work in 2006 and 2007, is a collaborative project of the Greek Archaeological Service, 39th Ephoreia in Tripolis, the University of Pennsylvania Museum of Archaeology and Anthropology, and the University of Arizona.

David Gilman Romano of the University of Pennsylvania Museum co-directs the project with Michaelis Petropoulos of the Greek Archaeological Service in Tripolis, and Mary Voyatzis of the University of Arizona.

High in the Arcadian mountains, the sanctuary at Mt. Lykaion was well known in antiquity as one of the most famous Zeus shrines in ancient Greece, as well as a site of early athletics in honor of the Greek’s greatest god. The site, which features an ancient hippodrome, a stadium and buildings related to the ancient athletic festival that rivaled the neighboring sanctuary of Zeus at Olympia, is known to have served as an important Pan Arcadian as well as Pan Hellenic Sanctuary that attracted pilgrims, athletes and dignitaries from all over the Greek world from the Archaic period to the Hellenistic period, ca. 700-200 BCE.

Last summer, a small excavation trench in the altar yielded Early, Middle and Late Helladic, ca. 3000-1200 BCE pottery sherds, indicating activity in this region from as early as 3000 BCE. The new material creates a vastly different account of the history of the altar and the site.

The intriguing discovery of one rock crystal lens-shaped seal bearing the image of a bull with full frontal face, likely of Late Minoan I or Late Minoan II date (1500-1400 BC), has, as of yet, no related materials to accompany it—but it does show at least some early connection between the two cultural areas.

Early 20th century excavations of the Greek Archaeological Society at the altar suggested the earliest activity there to be about 700 BCE, and the Mt. Lykaion Excavation and Survey Project excavation found much evidence for activity in later periods: pottery and objects from the Geometric, Archaic, Classical and Hellenistic periods (900-200 BCE), including miniature vases, bronze tripods and rings, iron blades, an iron spit, and silver coins, were excavated from the trench.

Several ancient authors mention that human sacrifice was practiced at the altar of Zeus—Pausanias alludes to mysterious sacrificial practices in his Descriptions of Greece—but to date, no evidence has been found. A considerable amount of animal bones was recovered from the altar excavations, with analysis underway, but preliminary results indicate large and small animal bones of various kinds, and no human bones.

The Mt. Lykaion Excavation and Survey Project boasts a Greek-American, interdisciplinary team of archaeologists, geologists, geophysicists, architects, topographical surveyors and students working throughout the site. The project will continue excavations at the altar, and other areas of the sanctuary, in 2008, with plans to continue work through 2010, and a long-range proposal under consideration to develop an archaeological park to unify and protect nearly 300 square kilometers of land in and around the site.

Two games were demonstrated at E3 this year for Project Natal: Ricochet, a Breakout style game where the player uses their whole body to hit balls through a wall of bricks down a corridor; and Paint Party, where users throw and splash paint on a virtual canvas to paint their own masterpiece. Whilst the artistic results appear more Jackson Pollock than Michelangelo at the moment (as well as featuring an elephant in Africa in every piece of material Microsoft has released), Paint Party appeared to respond well to Microsoft creative director Darren Bennett’s simple gesture and vocal commands.

Similar in concept to Sony’s PlayStation EyeToy, Project Natal differentiates itself by how accurate it seemed to be in comparison. Also Natal gives the user the ability to move around freely in any direction, and it can tell the difference between a user striking with their hand and moving forward. Those looking for concrete information on pricing, devices and release dates were disappointed, with Project Natal being described as a “concept of the future”, but we’re looking forward to some more solid information from Microsoft in the near future.

Meanwhile, Sony’s motion control system is more traditional than Project Natal. It incorporates a “wand”-like device for controlling in-game action, with the existing PlayStation Eye camera to record a player’s movements. Interestingly, players will be able to use two wands for motion that simulates dual-handed controls, like firing a bow and arrow, or using a sword and shield. Sony’s motion control scheme may lack the wow-factor of Microsoft’s Project Natal, but it apparently sports amazing accuracy.

It’s also impossible not to draw a comparison with Nintendo’s Wii motion system, the leading motion tracking system on the market and the most popular home games console to boot. Microsoft seemed to recognise this too, with Tsunoda making a dig at Nintendo users about how Ricochet “isn’t a game where you end up on the sofa just using some kind of preset waggle commands”. Microsoft also seems to believe that “the vast majority of people are just too intimidated to pick up a video game controller”, according to Steven Spielberg, who also announced he is working on several titles for the new system. Unlike Sony and Nintendo’s motion controlling systems, Project Natal is entirely controller free, but we’re cautious to see how well this truly translates to any Natal releases.

While Sony and Microsoft both debuted new systems for their assault on Nintendo’s domination of the video games market, today Nintendo only showed us more of the Wii Motion Plus attachment, which debuted last year at E3 2008, touting it as “a new sense of realism in gameplay” — obviously the company hadn’t seen Sony or Microsoft’s press conferences at that point. The Wii Motion Plus is the add-on that plugs into your Wii Remote, or Wiimote, to deliver the kind of accuracy and sensitivity it was believed the Wiimote would originally provide. It was announced today that Wii Motion can be used with Tiger Woods, Grand Slam Tennis and Sega’s Virtual Tennis. Nintendo may not have added anything new to the party this year, but it wasn’t necessary seeing as the company is already so deeply entrenched in the motion-sensing stake.

Liquid water is a key ingredient for life as we know it. The newfound planet is located at the “Goldilocks” distance-not too close and not too far from its star to keep water on its surface from freezing or vaporizing away.

And while astronomers are not yet able to look for signs of biology on the planet, the discovery is a milestone in planet detection and the search for extraterrestrial life, one with the potential to profoundly change our outlook on the universe.

“The goal is to find life on a planet like the Earth around a star like the Sun. This is a step in that direction,” said study leader Stephane Udry of the Geneva Observatory in Switzerland. “Each time you go one step forward you are very happy.”

The new planet is about 50 percent bigger than Earth and about five times more massive. The new “super-Earth” is called Gliese 581 C, after its star, Gliese 581, a diminutive red dwarf star located 20.5 light-years away that is about one-third as massive as the Sun.

Smallest to date

Gliese 581 C is the smallest extrasolar planet, or “exoplanet,” discovered to date. It is located about 15 times closer to its star than Earth is to the Sun; one year on the planet is equal to 13 Earth days. Because red dwarfs, also known as M dwarfs, are about 50 times dimmer than the Sun and much cooler, their planets can orbit much closer to them while still remaining within their habitable zones, the spherical region around a star within which a planet’s temperature can sustain liquid water on its surface.

Because it lies within its star’s habitable zone and is relatively close to Earth, Gliese 581 C could be a very important target for future space missions dedicated to the search for extraterrestrial life, said study team member Xavier Delfosse of Grenoble University in France.

“On the treasure map of the universe, one would be tempted to mark this planet with an X,” Delfosse said.

Two other planets are known to inhabit the red dwarf system. One is a 15 Earth-mass “hot-Jupiter” gas planet discovered by the same team two years ago, which orbits even closer to its star than does Gliese 581 C. Another is an 8 Earth-mass planet discovered at the same time as Gliese 581 C, but which lies outside its star’s habitable zone.

Possible waterworld

Computer models predict Gliese 581 C is either a rocky planet like Earth or a waterworld covered entirely by oceans.

“We have estimated that the mean temperature of this super-Earth lies between 0 and 40 degrees Celsius [32 to 104 degrees Fahrenheit], and water would thus be liquid,” Udry said.

The scientists discovered the new world using the HARP instrument on the European Southern Observatory 3.6 meter telescope in La Sille, Chile. They employed the so-called radial velocity, or “wobble,” technique, in which the size and mass of a planet are determined based on small perturbations it induces in its parent star’s orbit via gravity.

Udry said there was a fair amount of time between the calculation of Gliese 581 C’s size and the realization it was within its star’s habitable zone. “That came at the end,” Udry said.

When it did hit him, Udry knew he would be spending time fielding phone calls from the media. “You right away think about the journalists who will like it very much.

More to come

David Charbonneau, an astronomer at the Harvard-Smithsonian Center for Astrophysics (CfA) who was not involved in the study, said the new finding is an “absolutely fantastic discovery.”

“It means there probably are many more such planets out there,” Charbonneau said in a telephone interview. Whether Gliese 581 C harbors life is still unknown, but “it satisfies for the first time a key requirement.”

Charbonneau also praised the team’s technical skills. “The wobble induced on the star by each of these planets is really tiny-it’s just a few meters a second. That means their measurement precision is exquisite,” he said.

David Latham, another astronomer at Harvard-Smithsonian CfA, echoed other scientists’ praise of the discovery but said the next step is to find a similar world where the orbit of the habitable planet carries it between Earth and its parent star. This will allow scientists to observe it using the transit technique, whereby the small dimming starlight caused by the planet’s passage across the face of its sun can be used to calculate its size.

Only then can scientists determine for certain whether the world is rocky or covered by water, Latham said.

Alan Boss, a planetary theorist at the Carnegie Institution of Washington, said the new planet’s potential for liquid water made it “fascinating.” Gliese 581 C “is the closest planet to another Earth that has been found to date. I hope the SETI folks are listening,” Boss said.

Seth Shostak, a senior astronomer at the SETI institute, said the Gliese 581 system has in fact been looked at twice before for signs of intelligent life. The first time was in 1995 using the Parkes Radio Telescope in Australia; the second time occured in 1997 using the 140-foot telescope in Greenbank,West Virgina. Both times revealed nothing.

“It has been looked at twice, but that doesn’t mean we shouldn’t look at it again,” Shostak said. “And indeed we should because this is the best candidate the extrasolar planet guys have come up with yet.”

Shostak said he was “jazzed” by the discovery. “This is pointing to something that in the past has only been an assumption, namely that Earth-sized worlds are not rare,” he said. “We know of only two [planets in the habitable zone]. We know this one and we know our own. But two is better than one.”

Shostak said the Gliese 581 system will likely be looked at again over much wider range of the radio spectrum when the new Allen Telescope Array begins operations this summer.

Selama ini hampir semua orang sangat bergantung pada hasil indeks
pemeriksaan fungsi hati (Liver Function Index). Mereka menganggap bila
pemeriksaan menunjukkan hasil index yang normal berarti semua OK.
Kesalahpahaman macam ini ternyata juga dilakukan oleh banyak dokter
spesialis. Benar-benar mengejutkan, para dokter yang seharusnya
memberikan pengetahuan yang benar pada masyarakat umum, ternyata
memiliki pengetahuan yang tidak benar. Pencegahan kanker hati harus
dilakukan dengan cara yang benar. Tidak ada jalan lain kecuali
mendeteksi dan mengobatinya sedini mungkin, demikian kata dokter Hsu
Chin Ch’uan. Tetapi ironisnya, ternyata dokter yang menangani kanker
hati juga bisa memiliki pandangan yang salah, bahkan menyesatkan
masyarakat, inilah penyebab terbesar kenapa kanker hati sulit untuk
disembuhkan.

Saat ini ada seorang pasien dokter Hsu yang mengeluh bahwa selama satu
bulan terakhir sering mengalami sakit perut dan berat badannya turun
sangat banyak. Setelah dilakukan pemeriksaan supersound baru diketemukan
adanya kanker hati yang sangat besar, hampir 80% dari livernya (hati)
sudah termakan habis. Pasien sangat terperanjat, “Bagaimana mungkin?
Tahun lalu baru melakukan medical check-up dan hasilnya semua normal.
Bagaimana mungkin hanya dalam waktu satu tahun yang relatif singkat bisa
tumbuh kanker hati yang demikian besar?”

Ternyata check-up yang dilakukannya hanya memeriksa fungsi hati. Hasil
pemeriksaan juga menunjukkan “normal”. Pemeriksaan fungsi hati adalah
salah satu item pemeriksaan hati  yang paling dikenal oleh masyarakat.
Tetapi item  ini pula yang paling disalahpahami oleh masyarakat kita
(Taiwan).

Pada umumnya orang beranggapan bahwa bila hasil index pemeriksaan fungsi
hati menunjukkan angka normal berarti tidak ada masalah dengan hati.
Tetapi  pandangan ini mengakibatkan munculnya kisah-kisah sedih karena
hilangnya kesempatan mendeteksi kanker sejak stadium awal.

Dokter Hsu mengatakan, GOT dan GPT adalah enzim yang paling banyak
ditemui di dalam sel-sel hati. Bila terjadi radang hati atau karena satu
dan sebab lain sehingga sel-sel hati mati, maka GOT dan GPT akan lari
keluar. Hal ini menyebabkan kandungan GOT dan GPT di dalam darah
meningkat. Tetapi tidak  adanya peningkatan angka GOT dan GPT bukan
berarti tidak terjadi pengerasan pada hati atau tidak adanya kanker
hati. Bagi banyak para penderita radang  hati, meski kondisi radang hati
mereka telah berhenti, tetapi dalam hati (liver) mereka telah terbentuk
serat-serat dan pengerasan hati. Dengan  terbentuknya pengerasan hati,
maka akan mudah sekali untuk timbul kanker  hati.

Selain itu, pada stadium awal kanker hati, index hati juga tidak akan
mengalami kenaikan. Karena pada masa-masa pertumbuhan kanker, hanya
sel-sel  di sekitarnya yang diserang sehingga rusak dan mati. Karena
kerusakan ini  hanya secara skala kecil maka angka GOT dan GPT mungkin
masih dalam batas  normal, katakanlah naik pun tidak akan terjadi
kenaikan yang tinggi.
Tetapi oleh karena banyak orang yang tidak mengerti akan hal ini
sehingga berakibat  terjadilah banyak kisah sedih.

Penyebab utama kerusakan hati adalah :

1. Tidur terlalu malam dan bangun terlalu siang adalah penyebab paling
utama.
2. Tidak buang air di pagi hari.
3. Pola makan yang terlalu berlebihan.
4. Tidak makan pagi.
5.  Terlalu banyak mengkonsumsi obat-obatan.
6. Terlalu banyak mengkonsumsi bahan pengawet, zat tambahan, zat
pewarna, pemanis buatan.
7.  Minyak goreng yang tidak sehat. Sedapat mungkin kurangi penggunaan
minyak goreng saat menggoreng makanan, hal ini juga berlaku meski
menggunakan minyak goreng terbaik sekalipun seperti olive oil. Jangan
mengkomsumsi makanan yang digoreng bila kita dalam kondisi penat,
kecuali dalam kondisi tubuh yang fit.
8.  Mengkonsumsi masakan mentah (sangat matang) juga menambah beban
hati. Sayur mayur dimakan mentah atau dimasak matang 3 - 5 bagian. Sayur
yang digoreng harus dimakan habis saat itu juga, jangan disimpan.

Kita harus melakukan pencegahan dengan tanpa mengeluarkan biaya tambahan.
Cukup atur gaya hidup dan pola makanan sehari-hari. Perawatan dari pola
makan dan kondisi waktu sangat diperlukan agar tubuh kita dapat
melakukan penyerapan dan pembuangan zat-zat yang tidak berguna sesuai
dengan “jadwalnya”.

* With its super slim, stylish design, massive 2GB music storage capacity, and 3.2 megapixel camera, the W890 Walkman® phone promises to hit the right notes with sophisticated music lovers and design connoisseurs alike.
* For the music fan on the move, the W380 Walkman® phone combines a unique clamshell design with all the music cred users expect from Sony Ericsson’s Walkman® phones. The phone packs in never-seen before features, including Gesture control which allows users to mute calls with a wave of their hands. There is also an external display that comes to life only when you need it; to show the name of a music track or to let you know who is calling.

“With these latest phones, we address the needs of young, fashion-conscious music lovers with the W380, as well as music connoisseurs who demand the latest Walkman® features and fast downloads offered by the W890,” says Ben Padley, Head of Music Marketing at Sony Ericsson. “These Walkman® phones combine Sony Ericsson’s undeniable expertise in mobile communications and mobile music to stunning effect.”

Sony Ericsson W890 Walkman® phone

* Choose music to match your mood with SensMe™
* Store up to 1800 tracks* with 2GB of memory
* Look sharp with a 3.2 megapixel camera
* All within a design as slim as a CD case

Unleash your inner DJ

Whether you’re on your own or with friends, the W890’s colour matched stereo headset and in-built stereo speakers deliver a high quality listening experience. The phone incorporates the Walkman® Player 3.0, the latest in Walkman® technology, which offers one-click access to the player and simple, intuitive navigation around your music.

Not only can you organise your tracks by artist, album, or visually using Album Art (the album’s front cover artwork) – with the W890, you can even select your music to match your mood. The SensMe™ music experience automatically plots your music by tempo and mood – letting you create a playlist that matches how you feel.

The W890 Walkman® phone offers the benefit of an expandable memory, which can be upgraded as your music collection grows. A 2GB Memory Stick Micro™ (M2™) is provided in-box - that equates to storage for up to 1800 songs*. If you tire of these, tune in to your favourite station using the W890’s FM Radio.

Download music and web pages – fast!
The W890’s HSDPA capabilities allow you to download music at speeds up to four times faster than with regular 3G devices. Plus, it makes viewing pages on the internet quicker and easier too. The phone is fully compatible with Sony Ericsson’s PlayNow™ mobile entertainment experience. This provides you with instant access to the latest content – whether it’s the full-length music tracks, the hottest mobile games, ringtones or wallpapers – downloadable either direct to your phone or via your PC.

Music without wires
Need to provide the music for a party on the spur of the moment? No problem. As well as its own internal stereo speakers, the W890 is fully compatible with a range of the latest Sony Ericsson music accessories, including the Portable Bluetooth™ Speaker MBS-100 and the Stereo Bluetooth™ Headset HBH-DS220.

Match your personal lifestyle
With understated elegance, smooth curves and a choice of two stylish colours (Mocha Brown and Sparkling Silver), the W890 Walkman® phone will truly complement your personal style.

The W890’s 3.2 megapixel camera allows you to record the moment for posterity. One-press access to the camera means you need never miss a shot. Plus, instantly upload your photos to your personal online gallery, or ‘blogsite’, to let your friends know what you’re up to.

The W890 Walkman® phone is a HSDPA/UMTS 2100 and GSM/EDGE 850/900/1800/1900 phone and will be available in selected markets from Q1 2008. The W898c Walkman® phone is a GSM/EDGE 850/900/1800/1900 phone for the China market only.

Sony Ericsson W380 Walkman® phone

* Walkman® controls on top – see what’s playing and manage your music without even opening the phone
* Gesture Control – mute calls or silence the alarm with a wave of your hand
* TrackID™ – record a clip from the radio and identify the song, singer and album instantly.

Hear it, Name it, Play it, Get it
The W380 Walkman® phone comes complete with Media Manager PC software that lets you easily transfer your music, photos and videos between your computer and phone. Simply point, click and drag your music files from your computer to your phone – the software automatically converts your music to the right format.

Store hours of your favourite music (up to 271 songs*) on the W380’s 512 MB Memory Stick Micro™ (M2™) or tune in to your favourite FM radio station.

Hear a song on the radio you don’t recognise but really like? Use the W380’s TrackID™ feature to tag a clip from the phone’s radio (or any external source) and find out instantly who sings it, what it’s called and which album it’s from. The TrackID™ functionality, available on the W380, the W890 and a host of other Walkman® phones – is one of the phones’ most popular features. Latest figures show that every second, someone, somewhere, is using TrackID™ to identify a song they love.

Once you have identified the song, get it onto your phone in just a few clicks via PlayNow™. Or browse through the latest full-length music tracks, mobile games, MP3 ringtones and wallpapers – all available from PlayNow™ straight to your W380 Walkman® phone or via your PC.

Take it to the top
The W380 Walkman® phone brings your music to the surface of the phone, allowing you to control what you’re listening to without needing to open the phone. Skip forward or backwards between tracks or pause the music effortlessly. One-touch buttons on the top of the phone light up when the Walkman® player is switched on and a hidden display comes to life, providing track information at a glance.

When not in use, the W380 Walkman® phone looks discreet and laid-back from the outside. But as soon as you receive a call or play music, it comes alive. Choose different light effects for different callers, and see your music ‘dance’ when the phone’s lights match the beat of your favourite song.

Keep your hands off!
Mute your phone with a wave of your hand. Or snooze the alarm if you’re lying in bed. The W380’s Gesture Control feature allows true ‘handsfree’ handling of your calls for the first time – show it off to your friends!

Accessorise it
To enjoy your music discreetly when you’re in public, choose a great headset to go with it. Pick from the Stereo Portable Headset HPM-83 or the Stereo Bluetooth™ Headset HBH-DS200 if you want to stream music wirelessly from your phone.

The W380 is a GSM/EDGE/GPRS 850/1800/1900 and 900/1800/1900 clamshell phone and will be available in selected markets from Q1 2008.

* assumes eAAC+ encoded files.

Legal Information
* Assumes 3G broadband (HSDPA) connection and the download of an average full track 4 minute song.
1) Facts and features may vary depending on local variant.
2) Talk and standby times are affected by network preferences, type of SIM card, connected accessories and various activities e.g. games. Kit contents and colour options may differ from market to market. The full range of accessories may not be available in every market.
© Sony Ericsson Mobile Communications AB, 2007.
The liquid identity logo, TrackID, PlayNow and M-Buzz are trademarks or registered trademarks of Sony Ericsson Mobile Communications AB. Sony, Walkman and the Walkman logo are trademarks or registered trademarks of Sony Corporation.
Ericsson is the trademark or registered trademark of Telefonaktiebolaget LM Ericsson.
TrackID and Media Manager are powered by Gracenote Mobile MusicID. Gracenote and Gracenote Mobile MusicID are trademarks of Gracenote, Inc.
Bluetooth is a trademark or registered trademark of Bluetooth SIG Inc.
Picture blogging and video blogging are powered by Blogger. Blogger is a trademark or registered trademark of Google Inc. Google is a trademark or registered trademark of Google Inc.
Java and all Java-based trademarks and logos are trademarks or registered trademarks of Sun Microsystems, Inc.
Microsoft and ActiveSync are trademarks of the Microsoft group of companies
Other product and company names mentioned herein may be the trademarks of their respective owners.
Any rights not expressly granted herein are reserved.
Subject to change without prior notice.

Sony Ericsson Mobile Communications was established as a 50:50 joint venture by Sony and Ericsson in October 2001, with global corporate functions located in London. The company serves the worldwide communications market with innovative and feature-rich mobile phones, accessories and PC-cards, and it has R&D sites in Europe, Japan, China, India and America. Sony Ericsson is the title sponsor of the Women’s Tennis Association, and works with the Association to promote the Sony Ericsson WTA Tour in over 80 cities during the year. For more information, please visit www.SonyEricsson.com

Harian Jerman Tagesspiegel yang terbit di Berlin menulis:

Di Kairo Obama memberi pidato yang kuat dan bernuansa. Dengan meyakinkan ia memberi uluran tangan. Memang ada harapan cukup tinggi sebelum pidato itu. Antara lain karena asal-usul Obama sendiri, biografinya dan janji-janji politiknya. Hubungan kompleks antara Amerika Serikat dan dunia Islam tentu tidak bisa diperbaiki hanya dalam satu hari saja. Namun penampilan Obama di Kairo telah memberi impuls penting.

Harian Perancis Liberation memuji pidato Obama sebagai titik balik politik Amerika Serikat dalam hubungan dengan dunia Islam. Harian ini dalam tajuknya menulis:

Dunia Islam tidak boleh direduksi hanya sebagai terorisme dan fanatisme. Kata-kata tegas Obama ini mendapat sambutan positif di dunia Islam, dan menandai titik balik dalam politik luar negeri Amerika Serikat. Obama tidak mencoba menutupi latar belakangnya yang beragam. Ia bangga menjadi warga Amerika Serikat. Ia menghargai agama ayahnya. Obama menemukan kata-kata yang tepat bagi warga Yahudi dan Palestina. Ia mengecam segala bentuk penolakan terhadap eksistensi Israel, pada saat yang sama ia menggarisbawahi hak warga Palestina atas sebuah negara sendiri. Kepada semua pihak, Obama menyampaikan fakta. Dengan demikian, ia mengingatkan semua pihak tentang tanggung jawab mereka.

Harian Inggris Daily Telegraph berkomentar:

Presiden Amerika Serikat menerangkan kesediaannya untuk memperbaiki hubungan dengan dunia Islam. Namun adakah kapasitas untuk berdialog secara rasional di Timur Tengah? Ataukah fundamentalisme sudah demikian menggerogoti dunia Islam, sehingga kebanyakan dari mereka tidak akan menerima eksistensi Israel, atau menghilangkan prasangka terhadap Barat? Sedangkan di pihak Israel, masalahnya adalah, apakah konsesi-konsesi yang diperlukan untuk proses perdamaian bisa diterima secara politis. Misalnya saja pembagian kota Yerusalem. Obama menunjukkan bahwa ia tetap percaya pada penduduk Timur Tengah. Semoga warga Timur Tengah pun bisa saling percaya danpunya kebesaran hati semacam itu.

Harian Italia Corriere della Sera menulis:

Ini adalah pidato yang ditunggu-tunggu. Dengan kata-kata jelas dan gamblang, Obama memaparkan butir demi butir sengketa antara Israel dan Palestina. Obama tidak memberi agenda, namun menegaskan lagi prinsip dua negara, yang harus hidup berdampingan secara damai. Amerika Serikat memang punya hubungan khusus dengan Israel, namun ini bukan cek kosong bagi Israel. Di lain pihak, Hamas harus menghentikan kekerasan dan mengakui eksistensi Israel, jika ingin berdiri sama tinggi.