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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The question of whether prosthesis/abutment tooth interface debonding is associated with inappropriate occlusal force is investigated in this study. A new modeling approach was employed to perform the interfacial stress analyses. Solid models of resin-bonded (RB) prosthesis and abutment teeth were constructed by stacking serious section contours that were obtained from CT images. A 3-D finite element (FE) model of RB prosthesis/abutment teeth was generated in a CAD system after assembling and meshing procedures. An in-house program was developed to combine the FE package (ANSYS) to calculate the interfacial (normal and shear) stresses at the prosthesis/molar interface with the bonding and debonding conditions. After 10 different occlusal force(s) evaluations, three initial opening gaps at the distal margin of the retainer were assumed to examine the possible interface debonding mechanism under the worst loading case. The results indicated that a more accurate FE model of the posterior RB prosthesis/abutments could be generated through combining several computer-aided techniques. The maximum interfacial stresses were obtained when the occlusal force was applied on the buccal slope of the distolingual cusp of the molar. For interface debonding simulations, peak normal and shear stresses were found near the debonding areas and stress values increased gradually with small to large initial opening gaps. From these results, prosthesis/abutment tooth interfacial fatigue damage might arise or accelerate the interface to debond under adequate bonding or initial gap opening conditions after long-term repeated inappropriate occlusal force actions.
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PMID:Integration of CT, CAD system and finite element method to investigate interfacial stresses of resin-bonded prosthesis. 1285 Feb 97

The incidence of obesity has increased dramatically in recent years, making it one of the most pressing public health concerns worldwide. Obesity is commonly associated with comorbid conditions, most notably diabetes, coronary artery disease, and hypertension, and the coexistence of these diseases has been termed the Metabolic Syndrome. The identification of the hormone leptin provided a molecular link to obesity. Leptin is recognized as the central mediator in an endocrine circuit regulating energy homeostasis. Leptin administration leads to hypophagia, increased energy expenditure, and weight loss, while leptin deficiency enacts an adaptive response to starvation manifested by hyperphagia, decreased energy expenditure, and suppression of the neuroendocrine axis. While elucidation of leptin's role has permitted a more detailed view of the biology underlying energy homeostasis, most obese individuals are leptin resistant. A more complete understanding of the molecular components of the leptin pathway is necessary to develop effective treatment for obesity and the Metabolic Syndrome. The identification and role of one such component, stearoyl-CoA desaturase-1 (SCD-1), is reviewed here. Leptin's actions are not due to its anorectic effects alone. Leptin also mediates specific metabolic effects, including the potent depletion of triglyceride from liver and other peripheral tissues. To explore the molecular basis by which leptin depletes hepatic lipid, we used oligonucleotide arrays to identify genes in liver whose expression was modulated by leptin treatment. An algorithm was created that identified and ranked genes specifically repressed by leptin. The gene ranking at the top of this list was SCD-1, the rate limiting enzyme in the biosynthesis of monounsaturated fats. SCD-1 was specifically repressed during leptin-mediated weight loss, and mice lacking SCD-1 showed markedly reduced adiposity on both a lean and ob/ob background (ab(J)/ab(J); ob/ob), despite higher food intake. ab(J)/ab(J); ob/ob mice also showed a complete correction of the hypometabolic phenotype and hepatic steatosis of ob/ob mice, suggesting that fatty acid oxidation is enhanced in the absence of SCD-1. These findings indicate that pharmacologic manipulation of SCD-1 may be of benefit in the treatment of obesity, diabetes, hepatic steatosis, and other components of the Metabolic Syndrome.
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PMID:Stearoyl-CoA desaturase-1 and the metabolic syndrome. 1468 58

The high-density lipoprotein (HDL)-Atherosclerosis Treatment Study showed that simvastatin plus niacin (mean daily dose 13 mg and 2.4 g, respectively) halt angiographic atherosclerosis progression and reduce major clinical events by 60% in patients with coronary artery disease (CAD) who have low HDL, in comparison with placebos, over 3 years. How safe and well-tolerated is this combination? One hundred sixty patients with CAD, including 25 with diabetes mellitus, with mean low-density lipoprotein cholesterol of 128 mg/dl, HDL cholesterol of < or =35 mg/dl (mean 31), and mean triglycerides of 217 mg/dl were randomized to 4 factorial combinations of antioxidant vitamins or their placebos and simvastatin plus niacin or their placebos. Patients were examined monthly or bimonthly for 38 months; side effects (gastrointestinal upset, nausea, anorexia, vision, skin, and energy problems, or muscle aches) were directly queried and recorded. Aspartate aminotransferase, creatine phosphokinase (CPK), uric acid, homocysteine, and fasting glucose levels were regularly monitored. A safety monitor reviewed all side effects and adjusted drug dosages accordingly. Patients who received simvastatin plus niacin and those on placebo had similar frequencies of clinical or laboratory side effects: any degree of flushing (30% vs 23%, p = NS), symptoms of fatigue, nausea, and/or muscle aches (9% vs 5%, p = NS), aspartate aminotransferase (SGOT) > or =3 times upper limit of normal (3% vs 1%, p = NS), CPK > or =2 times upper limit of normal (3% vs 4%, p = NS), CPK > or =5 times upper limit of normal, new onset of uric acid > or =7.5 mg/dl (18% vs 15%, p = NS), and homocysteine > or =15 micromol/L (9% vs 4%, p = NS). Glycemic control among diabetics declined mildly in the simvastatin-niacin group but returned to pretreatment levels at 8 months and remained stable for rest of the study. This combination regimen was repeatedly described by 91% of treated patients and 86% of placebo subjects as "very easy" or "fairly easy" to take. Thus, the simvastatin plus niacin regimen is effective, safe, and well tolerated in patients with or without diabetes mellitus.
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PMID:Safety and tolerability of simvastatin plus niacin in patients with coronary artery disease and low high-density lipoprotein cholesterol (The HDL Atherosclerosis Treatment Study). 1475 79

Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. Left ventricular hypertrophy and coronary artery disease are both often subclinical diseases in hypertensives. Symptomatic coronary artery disease in hypertension may be due to atherosclerosis in epicardial arteries, microvascular dysfunction, reduced fibrinolytic capacity, or left ventricular hypertrophy; the latter is present in 20-50% of patients with mild to moderate and in up to 90% of patients with severe hypertension. Left ventricular hypertrophy in hypertension is associated with a twofold increase in risk of myocardial infarction, sudden death and stroke, and a fourfold increase in risk of heart failure. While coronary artery disease is the most common cause of heart failure in men, hypertension and in particular untreated isolated systolic hypertension is the most common cause in women. Heart failure symptoms may be subtle in hypertension, like tiredness or reduced physical capacity. Echocardiography can reveal subclinical heart disease as well as serve as a guide to correct diagnosis and treatment.
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PMID:[Hypertension and heart disease]. 1503 15

Frovatriptan succinate is one of the most recent serotonin receptor agonists to receive FDA, approved labelling for use in the acute management of migraine with or without aura in adults. The mechanism of action of frovatriptan is thought to be similar to that of a serotonin agonist. However, frovatriptan has distinctive pharmacokinetic and pharmacologic properties, chiefly, a high affinity for serotonin receptors 1B and 1D and a long elimination half-life; frovatriptan was shown to be more selective for cerebral than coronary arteries, a property which makes frovatriptan more favourable in patients at risk of coronary artery disease. Additionally, frovatriptan has a half-life of approximately 25 h, substantially longer than that of any other agent within its class. This property makes frovatriptan suitable for patients who typically suffer migraines of long duration and/or those who suffer migraine recurrence. The efficacy of frovatriptan in the treatment of acute migraine was demonstrated in five double-blind, randomised, placebo-controlled trials. At 2h, headache response rates for frovatriptan 2.5 mg ranged from 38 to 40% compared to 22-35% for placebo. Headache recurrence for frovatriptan 2.5 mg at 24h ranged from 9 to 14% compared with 18% in placebo subjects. Frovatriptan has no clinically significant pharmacokinetic interactions with drugs used for migraine prophylaxis or with commonly prescribed medications. Adverse effects of frovatriptan including dizziness, paresthesia, dry mouth, fatigue and flushing were generally mild and well tolerated. Given the fact that patient response to serotonin agonists is individualised, and selecting an effective agent may involve trial and error, frovatriptan is a welcome alternative in the acute management of migraine.
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PMID:Frovatriptan succinate, a 5-HT1B/1D receptor agonist for migraine. 1531 27

Atrial fibrillation is the most common supraventricular tachyarrhythmia encountered in clinical practice, affecting over 5% of persons over the age of 65 years. A common pathophysiological mechanism for arrhythmia development is atrial distention and fibrosis induced by hypertension, coronary artery disease or ventricular dysfunction. Less frequently, atrial fibrillation is caused by mitral stenosis or other provocative factors such as thyrotoxicosis, pericarditis or alcohol intoxication. Depending on the extent of associated cardiovascular disease, atrial fibrillation may produce haemodynamic compromise, or symptoms such as palpitations, fatigue, chest pain or dyspnoea. Arrhythmia-induced atrial stasis can precipitate clot formation and the potential for subsequent thromboembolism. Comprehensive management of atrial fibrillation requires a multifaceted approach directed at controlling symptoms, protecting the patient from ischaemic stroke or peripheral embolism and possible conversion to or maintenance of sinus rhythm. Numerous randomised trials have demonstrated the efficacy of warfarin--and less so aspirin (acetylsalicylic acid)--in reducing the risk of embolic events. Furthermore, therapeutic strategies exist that can favourably modify symptoms by restoring and maintaining sinus rhythm with cardioversion and antiarrhythmic prophylaxis. However, the risks and benefits of various treatments is highly dependent on patient-specific features, emphasising the need for an individualised approach. This article reviews the findings of cost-effectiveness studies published over the past decade that have evaluated different components of treatment strategies for atrial fibrillation. These studies demonstrate the economic attractiveness of acute management options, long term warfarin prophylaxis, telemetry-guided initiation of antiarrhythmic therapy, approaches to restore and maintain sinus rhythm, and the potential role of transoesophageal echocardiographic screening for atrial thrombus prior to pharmacological or electrical cardioversion. Further, we discuss the merits and limitations of the cost-effectiveness analyses in the context of overall treatment strategies. Finally, we identify areas that will require additional research to achieve the goal of effective and economically efficient management of atrial fibrillation.
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PMID:Cost effectiveness of therapies for atrial fibrillation. A review. 1534 2

Physical inactivity is associated with alteration of normal physiologic processes leading to muscle atrophy, reduced exercise capacity, insulin resistance, and altered energy balance. Bed rest studies in human beings using stable isotopes of amino acids indicate that muscle unloading decreases the turnover rates of muscle and whole-body proteins, with a prevailing inhibition of protein synthesis. In the fasting state, muscle and whole-body nitrogen loss was not accelerated during bed rest. In experimental postprandial states, the amino acid-mediated stimulation of protein synthesis was impaired, whereas the ability of combined insulin and glucose infusion to decrease whole-body proteolysis was not affected by muscle inactivity. Thus, an impaired ability of protein/amino acid feeding to stimulate body protein synthesis is the major catabolic mechanism for the effect of bed rest on protein metabolism. This suggests that a protein intake level greater than normal could be required to achieve the same postprandial anabolic effect during muscle inactivity. Metabolic adaptation to muscle inactivity also involves development of resistance to the glucoregulatory action of insulin, decreased energy requirements, and increased insulin and leptin secretion. These alterations may lead to the development of the metabolic syndrome that is defined as the association of hyperinsulinemia, dyslipidemia, hypertension, hyperglycemia, and abdominal obesity. This cluster of metabolic abnormalities is a risk factor for coronary artery disease and stroke. Evidence indicates that exercise training programs may counteract all of these abnormalities both in healthy sedentary subjects and in patients affected by a variety of chronic disease states.
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PMID:Metabolic consequences of physical inactivity. 1564 7

Robust dental systems obtained by computer-aided design and manufacture (CAD/CAM) have been introduced and, in parallel, the strength of the ceramic materials used in fabricating dental crowns has improved. Yet all-ceramic crowns suffer from near-surface damage, limiting their clinical success, especially on posterior teeth. Factors directly associated with CAD/CAM fabrication that contribute to the degree of damage include material selection and machining parameters and strategies. However, a number of additional factors also either create new damage modes or exacerbate subcritical damage, potentially leading to catastrophic failure of the crown. Such factors include post-fabrication manipulations in the laboratory or by the clinician, fatigue associated with natural occlusal function, and stress fields created by compliance or distortion within the supporting tooth structure and/or adhesive material holding the crown to the tooth. Any damage reduces the strength of a crown, increasing the probability of catastrophic failure. The challenge is to understand and manage the combination of competing damage initiation sites and mechanisms, limitations imposed by the demand for aesthetics, and biologically related constraints.
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PMID:Near-surface damage--a persistent problem in crowns obtained by computer-aided design and manufacturing. 1605 Feb 14

Scleroderma heart involvement (SHI) is often manifest, and virtually always present when accurately searched and holds a significant prognostic value. Myocardial involvement by patchy fibrosis (secondary to both repeated ischaemia and immunoinflammatory damage) leads to ventricular diastolic dysfunction, whereas right ventricle overload and failure may complicate pulmonary hypertension. Left ventricular systolic dysfunction is present in a minority of patients, namely those presenting atherosclerotic coronary artery disease and/or arterial hypertension, sometimes triggered by sclerodermic renal involvement. Dysrhythmias and conduction disturbances are considered an hallmark of SHI, facilitated by autonomic dysfunction. SHI is frequently linked to parenchimal and/or vascular lung disease; they determine symptom occurrence, particularly dyspnoea, fatigue, palpitations and chest pain when pericardium is affected. Accurate cardiologic baseline screening and subsequent follow-up are mandatory in all patients, initially consisting in some noninvasive diagnostic procedures: visit, electrocardiogram (EKG), chest X-ray, Doppler-echocardiography. When needed, these examinations should be integrated by EKG Holter-monitoring, cardiopulmonary stress tests, cardiac magnetic resonance imaging, nuclear studies of myocardial function and perfusion, cardiac catheterization to better estimate pulmonary hypertension, and cardiac natriuretic hormone evaluation. Several vasodilator approaches (prostacycline or NO/endothelin) may counteract the microvascular dysfunction at peripheral and cardiopulmonary level, and fight the sequelae of pulmonary hypertension.
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PMID:Heart involvement and systemic sclerosis. 1621 71

Mitral regurgitation is the second most frequent reason for valve surgery. The most important causes of mitral regurgitation are degenerative valve disease (mitral valve prolapse), left ventricular impairment and dilatation (in coronary artery disease or dilated cardiomyopathy), and infective endocarditis. The regurgitation of blood from the left ventricle into the left atrium leads to dilatation of the left atrium, increase in pulmonary capillary pressure and pulmonary congestion. In chronic severe mitral regurgitation, the left ventricle dilates and becomes impaired over time. Key symptoms are fatigue and dyspnea on exertion. The most prominent physical sign is the characteristic systolic murmur. Echocardiography identifies severity, delineates morphology, and estimates the impact of mitral regurgitation on left ventricular function. Importantly, echocardiography identifies candidates for mitral valve repair. Symptomatic patients and asymptomatic patients with impaired left ventricular function should be operated. If possible, valve repair is preferred over valve replacement to better preserve left ventricular function and to avoid the need for postoperative anticoagulation (except if atrial fibrillation persists).
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PMID:[Mitral regurgitation]. 1628 35


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