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

Of 21 dogs from Sapporo, Hokkaido that had been recognised as having been bitten by ticks, 16 were seropositive to Borrelia burgdorferi by ELISA. Thirteen of the seropositive dogs showed signs such as fever, astasia, convulsions, anorexia, fatigue, abnormal gait, nervous signs, diarrhoea, corneal opacity and conjunctivitis. These signs subsided as a result of antibiotic treatment within five days. The plasma concentrations of creatinine in the 21 dogs were higher than in control dogs. Seven ticks that were removed from seven of the dogs were Ixodes persulcatus, and B burgdorferi was isolated from the midgut of two of the ticks.
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PMID:Canine Lyme disease: clinical and serological evaluations in 21 dogs in Japan. 800 99

Manifestations of chronic venous insufficiency of the lower limbs are related to congenital or acquired stasis in the deep veins, to post-phlebitis occlusion of the deep veins or to stasis in the superficial veins. Functional impairment may be associated with varicose veins or not. Clinical signs include a heavy feeling in the legs, fatigue, and sometimes cramps or impatience in the evening. Sometimes there is a seasonal character to the complaints. The varicosities are localized in the territory of the medial saphenous vein, the lateral saphenous vein, or both and sometimes affect the pelvic region. Complications may occur including hemorrhage of the varicose veins, superficial phlebitis or orthostatic hypotension. An echo coupled Doppler helps determine the therapeutic indications and provides a mapping of the venous system for functional evaluations. Varicose veins result from minute dilatations of superficial vessels. There are exclusively of aesthetic importance. Chronic venous insufficiency can lead to permanent or intermittant oedema of the lower limbs without inflammation. When permanent, a large cold leg fits into a suggestive clinical picture non venous causes of oedema can be determined with an ultrasound exploration. Postphlebitic reactions are the most frequent causes of large cold lower limbs due to venous insufficiency. Poor cutaneous trophism of venous origin includes dermo-epidermitis, pigmented purpura dermitis, capillary ectasia, leukoderma, sclerodermiform hypodermitis and leg ulcers. Superficial venous ulcers are often quite large, painless and chronic. Their prevalence increases with age. Venous ulcers are more often secondary to phlebitis than to varicose veins. The socio-economic impact is great.
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PMID:[Chronic venous insufficiency: clinical aspects]. 817 72

A model of isometric force production by skeletal muscle was developed in which the response to each stimulus in a train was described by a critically damped, linear second-order system. The parameters describing the system were constrained to be constant within an interstimulus interval, but were allowed to vary between interstimulus intervals. The ability of this model to match experimental data, and the time variation in the parameters (low-frequency gain and natural frequency) required to do so were examined in soleus and plantaris muscles of the cat stimulated by synchronous whole-nerve stimulation. The model produced good fits across firing rates from twitch to tetanus for slow and fast muscle, rested and fatigued muscle, and maximal submaximal stimulation. Both gain and natural frequency generally varied smoothly and predictably under all conditions. Gain increased at intermediate stimulation rates and in potentiated muscle, and decreased with fatigue and submaximal stimulation. Natural frequency was higher in fast muscle, and decreased with stimulation rate and fatigue. This modeling approach may provide a useful alternative to current models of skeletal muscle force, as its implementation is simple and it can describe force under conditions (fatigue, potentiation) where the muscle dynamics change with time.
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PMID:A linear time-varying model of force generation in skeletal muscle. 829 24

Spatial frequency adaptation is shown to cause a decrease in the exponent of the power law describing contrast increment thresholds. Next we show that spatial frequency adaptation produces almost no threshold elevation at a 30 msec test duration but a normal threshold elevation at 500 msec. Control experiments rule out an explanation in terms of sustained and transient mechanisms. Together these results show that spatial frequency adaptation cannot result from neuronal fatigue. The data can be explained by a contrast gain control network in which unit responses provide feedback signals that divide input contrast. Adaptation is hypothesized to produce an increase in the strength of this divisive feedback via temporary synaptic modification. A simple network model fits the data and also predicts both the magnitude and temporal dependence of the tilt aftereffect.
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PMID:Spatial frequency adaptation and contrast gain control. 850 53

Primary Generalized Epilepsy (PGE) has been more hotly debated over the past decades than other forms of epileptic seizure disorder. The sudden synchronous appearance of bilateral spikes and spike-waves (mainly with myoclonus resp. absence) used to perplex the earliest generation of electroencephalographers, and the enigmatic genesis of these discharges (and seizures) has not ceased to fascinate the investigators of this phenomenon. A "centrencephalic" concept with paroxysmal discharges arising from thalamic structures and "projecting" to the cortex was championed for many years and eventually laid aside. More recently, the role of the thalamic level has been re-emphasized, mainly on the basis of experimental work. In this article, the bulk of experimental work is critically reviewed: the simian model (Papio papio), the feline, and the rodent models (Wistar rat, tottering mouse). Stress is being laid on fundamental differences between all of these models and human PGE. EEG evidence indicates a superior frontal origin of bilateral-synchronous spikes and spike-waves; depth EEG recordings in patients have failed to demonstrate primary thalamic spike generation. The heart of the matter in PGE appears to be the mechanism underlying paroxysmal discharges; above all the role of arousal. It is not awakening from sleep but the ensuing period that is critical in its epileptogenic thrust caused by alternating periods of return to drowsiness and arousing stimuli. This biphasic process gradually escalates EEG bursts to myoclonus (or absences) and possibly to a generalized tonic-clonic convulsion. Most conducive to this crescendo is the state of tiredness following a night of poor sleep. Bilateral synchrony is not precise and small time differences exist. The line between primary and secondary bilateral synchrony (with a primary cortical focus) can become blurred. Genetic predisposition to generalized paroxysms must always be considered, even in the face of a primary focus with secondary bilateral synchrony. Photosensitivity is a second paroxysm-inducing mechanism in PGE; it is much less common than the abnormal arousal ("dyshormia"); both mechanisms can be present in the same patient. Therapy and prevention of seizures in PGE are finally discussed. The concept of abnormal arousal mechanisms can be put into practice in order to prevent seizures: avoidance of sleepless nights, not always an easy task in adolescents and young adults.
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PMID:Primary (idiopathic) generalized epilepsy and underlying mechanisms. 871 97

A general finding is that muscle activity leads to potassium fluxes across the muscle membrane as well as to muscle fatigue, defined as a reduction in the force-generating capacity of the muscle. However, much controversy exists regarding the causal role of potassium in fatigue development. The experimental model used is decisive in this context, e.g. whether we study intact in vivo organs in situ with voluntary contractions and reflex feedback for cardiorespiratory regulation, or whether we study in vitro isolated muscles or cells-or even skinned fibres. In the latter models, clear evidence has been presented that Ca2+ is the variable significant for force development and that K+ may be ignored. However, in the in situ situation the limiting link in the chain leading to muscle contraction may be one preventing the Ca2+ release from taking place. The sites are the triads, T-tubules, and the surface membrane. The function of the latter two regarding action potential amplitude and propagation depends on [K+] gradients. Again, conflicting results exist regarding the electrophysiological changes and [K+] in fatigue. The activity pattern must then be taken into consideration. During high-intensity (high-frequency) activity the increased interstitial [K+] has been demonstrated to relate to fatigue, while in low-intensity fatiguing protocols, the T-tubule may be the limiting site. This fits with the concept of interstitial [K+] playing an essential role as a regulatory feedback mechanism, e.g. adjusting muscle blood flow to the metabolic load during muscle activity.
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PMID:Potassium and fatigue: the pros and cons. 872 85

An analytic method based on simulation and modeling of long-term 45Ca2+ efflux data was used to estimate Ca2+ contents (nmol Ca2+/g tissue wet wt) and exchange fluxes (nmol Ca2+.min-1.g-1) for extracellular and intracellular compartments in in vitro hamster diaphragm. Three physiological states were studied: control (n = 5), acute fatigue (after repeated tetany; n = 5), and long-lasting fatigue (1-h recovery; n = 5). Experimental muscles were loaded with 45Ca2+ for 1 h, and efflux data were collected for 8 h by use of a flow-through tissue chamber. Induction of acute diaphragm fatigue led to a uniform 200% elevation of the 8-h efflux curve (expressed as dpm.min-1.mg-1) relative to control. Conversely, in long-lasting fatigue the early component of the efflux curve was depressed compared with control, whereas the balance of the curve was restored to baseline. Analysis of control efflux data revealed that the early curve (0-2 h) contained data on two rapidly exchanging extracellular Ca2+ compartments, whereas the late curve (2-8 h) reflected information on two slowly exchanging intracellular compartments. Modeling of acute fatigue efflux data estimated a 239% increase in one extracellular Ca2+ compartment (putative t-tubular membrane) and a 546% increase in one intracellular Ca2+ compartment (putative terminal cisternae). These increase accounted for the model prediction of a twofold rise in total diaphragm Ca2+. The kinetic data were quantitatively consistent with the hypothesis that diaphragm Ca2+ overload in acute fatigue required sarcolemmal Ca2+ permeability to double and Ca2+ diffusion into the t-tubular and terminal cisternal compartments to escalate nearly threefold. Fitting of long-lasting fatigue efflux data was associated with the sole prediction that t-tubular membrane Ca2+ was reduced to less than one-half of the control value.
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PMID:Compartmental analysis of Ca2+ kinetics in long-lasting diaphragm fatigue: loss of t-tubular membrane Ca2+. 880 8

Eight male patients with heart transplants at least a year after the operation were submitted to a 6-wk endurance training program and explored for their blood lactate kinetics before and after exercise. The tests consisted of a bicycle exercise upgraded by 20 W every 2 min until volitional fatigue. Training induced a significant (P < 0.025) decrease in lactate concentrations from the 40-W to the 120-W exercise step and a significant increase (P < 0.025) in the time into exercise (9.87 +/- 0.87 min vs 7.17 +/- 0.90 min) at which a lactate concentration of 2 mmol.l-1 was reached. Lactate recovery curves were significantly lower (P < 0.036) after training than before training, except at minutes 1, 2, 8, and 60. The fits of a biexponential mathematical model to the lactate recovery curves reveal a significant (P < 0.036) training-induced increase (+71%) in the slow-velocity constant gamma 2v of the model. In view of the functional meaning given to this parameter, namely the ability to remove lactate, it is concluded that training lowers blood lactate concentrations during exercise and recovery in patients with heart transplants at least in part by raising the efficiency with which lactate is removed, and that the ability to remove lactate can be a valuable criterion to evaluate physical fitness.
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PMID:Short endurance training improves lactate removal ability in patients with heart transplants. 883 32

If self-regulation conforms to an energy or strength model, then self-control should be impaired by prior exertion. In Study 1, trying to regulate one's emotional response to an upsetting movie was followed by a decrease in physical stamina. In Study 2, suppressing forbidden thoughts led to a subsequent tendency to give up quickly on unsolvable anagrams. In Study 3, suppressing thoughts impaired subsequent efforts to control the expression of amusement and enjoyment. In Study 4, autobiographical accounts of successful versus failed emotional control linked prior regulatory demands and fatigue to self-regulatory failure. A strength model of self-regulation fits the data better than activation, priming, skill, or constant capacity models of self-regulation.
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PMID:Self-control as limited resource: regulatory depletion patterns. 952 19

Many bones within the axial and appendicular skeleton are subjected to repetitive, cyclic loading during the course of ordinary daily activities. If this repetitive loading is of sufficient magnitude or duration, fatigue failure of the bone tissue may result. In clinical orthopedics, trabecular fatigue fractures are observed as compressive stress fractures in the proximal femur, vertebrae, calcaneus and tibia, and are often preceded by buckling and bending of microstructural elements. However, the relative importance of bone density and architecture in the etiology of these fractures is poorly understood. The aim of the study was to investigate failure mechanisms of 3D trabecular bone using micro-computed tomography (microCT). Because of its nondestructive nature, microCT represents an ideal approach for performing not only static measurements of bone architecture but also dynamic measurements of failure initiation and propagation as well as damage accumulation. For the purpose of the study, a novel micro-compression device was devised to measure loaded trabecular bone specimens directly in a micro-tomographic system. The measurement window in the device was made of a radiolucent, highly stiff plastic to enable X-rays to penetrate the material. The micro-compressor has an outer diameter of 19 mm and a total length of 65 mm. The internal load chamber fits wet or dry bone specimens with maximal diameters of 9 mm and maximal lengths of 22 mm. For the actual measurement, first, the unloaded bone is measured in the microCT. Second, a load-displacement curve is recorded where the load is measured with an integrated mini-button load cell and the displacement is computed directly from the microCT scout-view. For each load case, a 3D snap-shot of the structure under load is taken providing 34 microm nominal resolution. Initial measurements included specimens from bovine tibiae and whale spine to investigate the influence of the structure type on the failure mechanism. In a rod-like type of architecture as seen in the whale spine, structural failure was described by an initial buckling and bending of structural elements followed by a collapse of the overloaded trabeculae. In the more plate-like bovine tibial architecture, buckling and bending could not be observed. Failure rather seemed to occur instantaneously. In conclusion, micro-compression in combination with 3D microCT allows visualization of failure initiation and propagation and monitoring of damage accumulation in a nondestructive way. We expect these findings to improve our understanding of the relative importance of density, architecture and load in the etiology of spontaneous fractures of the hip and the spine. Eventually, this improved understanding may lead to more successful approaches to the prevention of age-related fractures.
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PMID:Micro-compression: a novel technique for the nondestructive assessment of local bone failure. 1010 Sep 46


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