Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first case was a 63-year-old man with edema in the lower extremities, and the second case was a 78-year-old man complaining of general fatigue and loss of appetite. Both cases had bilateral hydronephrosis and renal failure due to ureteric obstruction. Both patients with histologically proven idiopathic retroperitoneal fibrosis were studied by magnetic resonance imaging (MRI). MRI was performed using a superconducting magnet operating at 0.5 tesla and spin echo images were obtained. The retroperitoneal fibrous plaque appeared at an intermediate intensity on T1 weighted image and at a high intensity on T2 weighted image. They underwent intraperitoneal ureteral transposition and postoperative administration of prednisolone. Although their renal functions and hydronephrosis improved after the treatments, the fibrous plaque was still observed on MRI. It was considered that MRI was an excellent method of choice in the diagnosis and follow-up of retroperitoneal fibrosis.
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PMID:[Magnetic resonance imaging for retroperitoneal fibrosis: report of two cases]. 237 36

Recent work has now clearly established that coronary arterial thrombosis is the direct cause of acute myocardial infarction. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation. Platelets are thus activated and the clotting cascade is initiated. It is as yet unclear why a previously stable atherosclerotic plaque should fissure or rupture. However, suggested mechanisms include release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque. The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Intracellular acidosis, loss of high-energy phosphates, reduced sensitivity of contractile proteins to calcium, and accumulation of inorganic phosphate and lipid, all occur within the ischemic myocyte. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity. Most of these alterations are reversible if ischemia is relieved promptly. Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.
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PMID:The pathophysiology of acute myocardial infarction. 266 57

Pathologic evidence indicates that thrombosis in coronary arteries is most frequently initiated by fissures in atheromatous plaques and that the associated hemorrhage induces platelet aggregation. Less frequently, thrombosis may be initiated by arterial spasm or by pathologic abnormalities affecting the platelets or the mechanisms of plasma coagulation. For the rational development of antithrombotic drugs on the basis of aggregation inhibitors, the cause (or causes) of plaque fissure and of the ensuing platelet aggregation need therefore to be elucidated. Our current research is based on the working hypothesis that fissuring occurs when plaques have acquired a particular composition that can be disrupted by the cumulative effect of continuously varying hemodynamic forces (reminiscent of fatigue failure in artificial materials), and that fissure-associated hemorrhage, like hemorrhage anywhere else, initiates platelet aggregation via a concurrence of hemodynamic and biochemical mechanisms. Detailed studies are currently being directed toward establishing the sequence of events that determine the contributions of adenosine diphosphate, thromboxane A2, and other endogenous agents in promoting hemostatic platelet aggregation in real life and, by implication, arterial thrombosis. Important recent evidence has demonstrated repeated thrombosis in unstable angina patients. In such patients, aspirin diminishes by about half the incidence of myocardial infarction and death. Presumably, it prevents the formation of platelet thrombi, which would tend to be produced in the turbulent blood flowing through arterial segments severely narrowed by hemorrhage plaques or in spasm. Several other platelet-active drugs are also under investigation.
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PMID:Polypharmacologic interactions in the management of thrombosis. 266 84

The characteristics of the air-powder abrasive device (APAD) was reviewed from the current dental literature and found to be an excellent alternative to traditional methods for stain and plaque removal. Access to crowded teeth, grooves and involved furcation areas are easily obtainable with less operator fatigue. The APAD slurry produces different root surface abrasiveness, depending on the method of use. Extended maintenance periods of exposed root surface using the APAD can result in an enormous loss of root structure. To avoid permanent damage of the root, the device should be used with overlapping strokes and root exposure to the APAD slurry should be minimized. The device can be used for total cementum removal with less operator fatigue and more reproducibility than with hand instruments, leaving smooth and clean surfaces. In addition, the device may be a valuable tool in the detoxification of root surfaces during periodontal surgery.
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PMID:The effectiveness of the air-powder abrasive device on the tooth and periodontium: an overview. 269 Nov 71

Six male volunteers, previously immunized with yellow fever vaccine, were inoculated subcutaneously with a live, attenuated dengue-2 virus (PR-159/S-1) candidate vaccine. Five recipients developed viremia 8 or 9 days after vaccination, which lasted 1 to 10 days. The onset of viremia was followed by fever in three people, transient leukopenia in four, and an erythematous rash in one. One volunteer developed an oral temperature of 38.8 degrees C with headache, myalgia, fatigue, and photophobia suggestive of mild dengue fever. All five viremic volunteers developed fourfold or greater rises in serum neutralizing antibody. The sixth volunteer, who had a low titer of preexisting dengue-2 neutralizing antibody, had no viremia, no symptoms, and a modest rise in hemagglutination inhibiting antibody. Virus isolates obtained from plasma retained the small-plaque and temperature-sensitive growth characteristics of the vaccine virus in vitro. In this study, the vaccine virus genetically stable and immunogenic and seemed sufficiently attenuated for additional testing in humans.
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PMID:Dengue-2 vaccine: virological, immunological, and clinical responses of six yellow fever-immune recipients. 721 69

Immature synapses, developing moth neuromuscular junctions, were studied using electro-physiological and ultrastructural techniques, and were compared with synapses from the flight muscles of adult moths. Neuromuscular junctions, formed by short side branches of the single fast motor axon, were assessed for functional state by stimulating the nerve and recording the endplate potential intracellularly from the muscle fibre. The muscle was then fixed and prepared for scanning, thin-section, and freeze-fracture microscopy. The immature stage differs from the adult by having very small (average 7.8 mV, compared with 20-30 mV), long duration ejp's that fatigue rapidly. The immature junctions are, however, only 13% shorter than those of the adult. Within the junction, the nerve terminal comes into direct contact with the muscle membrane in a series of oval patches separated by glial processes. These regions of apposition or 'plaques' in the immature synapse are about half the diameter of the adult plaques. In freeze-fractured material, the nerve terminal membrane in the plaque region bears an irregular band of particles on the cytoplasmic leaflet; the length of the band is essentially the same in the immature synapse as in the adult. This band marks the location of the active zone, an electron dense bar of the same length in thin section. The apposing external leaflet of the muscle membrane bears a patch of postsynaptic particles; the patch is much smaller than in the adult plaque. These immature patches, presumably representing clusters of receptors, range in size from a dozen particles to a hundred or more. We consider it likely that a lack of postsynaptic receptors may partially explain the very small ejp in the developing synapse, but that other factors may also be limiting. Desmosome-like contacts between glial cells and the muscle fibre were observed. Small wisps of electron dense material appear to bridge the extracellular space between the nerve terminal and the muscle fibre or between the glial processes and the muscle fibre in some locations. They are found in the same regions of the neuromuscular junction as small groups of large particles, suggesting that these two features are different aspects of the same structure. From their location one could hypothesize that they have either a mechanical function of stabilizing the glial invaginations, or a role in communication between the three types of developing cells.
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PMID:Membrane structures and physiology of an immature synapse. 731 Apr 65

The primary trigger mechanisms leading to coronary artery disease are largely unknown; however, consensus has been reached that unstable angina pectoris is always associated with acute pathological and anatomical changes in a plaque, most commonly in the form of a plaque fissure or rupture involving the fibrous luminal cap with thrombosis, hemorrhage and dissection. Rupture almost always occurs at the weakest part of the fibrous cap and leads to exposition of extracellular lipids and matrix, necrotic tissue and lipid-laden foam cells. The exact mechanisms of plaque rupture are not entirely known; it is possible, however, that they do represent fatigue breaks in the tissue. The clinical consequences of these events are unstable angina pectoris and myocardial infarction.
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PMID:[Pathological-anatomic basis of unstable angina pectoris]. 787 Dec 99

The purpose of this investigation was to test the hypothesis that cyclic flexion of the coronary arteries contributes to the progression of atherosclerotic plaques. Coronary arteriograms were evaluated in 33 unselected patients who underwent 2 studies over a period of 25 +/- 16 months (mean +/- SD). Among the 33 patients, 103 plaques were identified. Plaques that showed progression were compared with plaques that showed no progression. The angle of flexion that occurred during systole at the site of the plaque was measured on the first arteriogram. In comparing progression versus no progression, the interval between arteriograms was 29 +/- 18 versus 23 +/- 14 months (p = NS) and percent stenosis at the first arteriogram was 42 +/- 28 versus 45 +/- 19% (p = NS). Percent stenosis at the time of the second arteriogram among plaques that progressed was 78 +/- 21%, and by definition, it remained 45 +/- 19% among those that did not progress. Among arteries with plaques that showed a progression of stenosis, the angle of flexion during systole was 19 +/- 13 degrees versus 9 +/- 15 degrees among arteries with plaques that did not progress (p < 0.01). Linear regression showed that the correlation of the angle of flexion with percent change of stenosis was relatively low (r = 0.32) but statistically significant (p < 0.005). Mathematic modeling of flexible and stiff plaques showed stresses approximately 1.5 to 1.9 times greater with 20 degrees than with 10 degrees flexion. Stresses due to flexion were usually greatest proximal and distal to the plaque along the subendothelial layer of the inner wall of the curved vessel. Data show that the angle of cyclic flexion, and consequently the stresses due to cyclic flexion of the artery were greatest in the region of plaques that progressed over the period of observation. Such stresses may have contributed to tissue damage of fatigue resulting in a more rapid progression of the atheromatous plaques.
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PMID:Effects of cyclic flexion of coronary arteries on progression of atherosclerosis. 814 Oct 82

In summary, the sequence of endothelial plaque disruption, platelet activation, and thrombogenic factors--that is, the balance between the thrombolytic system and the coagulation system--determine which blood vessel will thrombose and which vessel will remain patent. It seems to me that although the soft plaque with the thin cap and lipid core laden with oxidized LDL-activated macrophages is more prone to rupture than the calcified, hard plaque, it is also the plaque that may regress when the patient is treated aggressively with lipid-lowering or antioxidant therapy. In addition, drugs that lower blood pressure and heart rate may also decrease the tendency of the "vulnerable" plaque to rupture by attenuating fatigue failure. Current and future research should be directed at identifying vulnerable plaques in the individual patient, so that measures can be taken to prevent plaque rupture.
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PMID:Vascular events responsible for thrombotic occlusion of a blood vessel. 826 51

This review focuses on select current articles chosen for their unique contribution to the literature in scaling and root planing. New studies suggest that thorough root debridement can be achieved without overinstrumentation using certain sonic and ultrasonic scalers. Evaluation of residual plaque and calculus after instrumentation with hand- and power-driven scalers showed sonic and ultrasonic scalers to be equivalent, and in some cases, superior to hand scaling. When modified ultrasonic inserts were compared with unmodified ultrasonic inserts and hand curets, the modified ultrasonic inserts produced smoother roots with the least amount of damage, better access to the bottom of the pocket, better calculus and plaque removal, less operator time, and less operator fatigue than did hand scaling or ultrasonics equipped with unmodified inserts.
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PMID:Scaling and root planing without overinstrumentation: hand versus power-driven scalers. 840 51


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