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This study applied EMG analysis methods to identify muscle group activity profiles and potential overload risks in powered wheelchair use.We quantified muscle effort and fatigue using EMG analysis methods during powered wheelchair manoeuvres by 10 multiple sclerosis patients. Video recordings of the different sub-tasks were related to information on surface EMG amplitude (rectified EMG) and spectral information (Median frequency) from M. trapezius, M. deltoideus (pars medius), M. deltoideus (pars anterior), M. pectoralis, M. biceps, M. triceps, wrist extensors and flexors, using Joint Analysis of EMG Spectrum and Amplitude (JASA analysis).Task durations and subjective data indicated that tasks requiring finer motor control took longer and were perceived as more difficult. Kinesiological functions of all muscle groups identified forward steering to be associated with activation of M. deltoideus (pars anterior), M. pectoralis, M. trapezius and M. deltoideus (pars medius); backwards steering with predominant activation of M. deltoideus (pars medius), M. biceps brachii and wrist flexors; left steering with maximal activation of M. biceps and wrist flexors, and right steering with maximal activation of M. triceps and wrist extensors. These profiles were confirmed in analysis of the functional tasks. JASA analysis documented muscle fatigue in the wrist extensors, whereas increased activation was found in M. trapezius, M. deltoideus (pars anterior) and wrist flexors.EMG based kinesiological analysis gives insight in muscle activity and fatigue during powered wheelchair manoeuvres.

The aggregation of gel-filtered human platelets induced by A23187 is very sensitive to inhibition by ethanol. Similarly when platelets preloaded with [3H]5-hydroxytryptamine ([3H]5HT) are studied in a superfusion system under conditions where aggregation is likely (high platelet density, presence of Ca2+) the rate of release of [3H]5HT induced by A23187 is reduced by the presence of ethanol. However when platelet aggregation is less likely (low platelet density, absence of Ca2+) ethanol does not reduce the rate of [3H]5HT efflux induced by A23187 in superfused platelets. In addition, in contrast to the effects of ethanol on platelet aggregation, the transformation of human red cells to echinocytes induced by A23187 is accelerated by the presence of ethanol. Similarly the increased efflux of 3H from superfused rat striatal slices preloaded with [3H]dopamine which is produced by A23187 is potentiated by ethanol. It is concluded that the inhibitory effect of ethanol on the action of A23187 may be confined to platelet aggregation. This may be because the mechanisms of action of either A23187 or ethanol on platelet aggregation differ from those on other cell functions.

Inositol monophosphatase can be modified at two sites by pyrene maleimide. These sites have been identified as Cys141 and Cys218. Stoichiometric addition of pyrene maleimide allows the sole modification of Cys218. The fluorescence of the pyrene moiety on the modified protein can be excited directly or by resonance energy transfer. The fluorescence properties of the pyrene group on Cys218 allows the interaction of ligands with the enzyme to be monitored. This feature has allowed dissociation constants for various metal ions to be determined and allowed the formation of various enzyme/ligand complexes to be observed. These studies have demonstrated that Mg2+ is required to support Pi binding and that Li+ interacts with a post‐catalytic complex which is only formed in the forward reaction.

The storage and transport of gases in coal is of tremendous importance in the utilisation of coalbeds, and in particular the recovery of methane. There is also increasing interest in the use of coal mines as sites for carbon dioxide sequestration to alleviate the potentially harmful effects of global warming. This paper demonstrates the use of magnetic resonance imaging to investigate the spatiotemporal dynamics of gas transport in coal. The presence of significant structural heterogeneities in the coal was observed. Dynamical effects displayed a broad range of time constants ranging from minutes to days.

Phospholipase C (PLC) activity was measured by the incorporation of [3H]-inositol into lipids and by the breakdown of [3H]-inositol-labelled phosphatidylinositols (PI) and polyphosphatidylinositols (PPI) to [3H]-inositol phosphates; phospholipase A2 (PLA2) activity by the breakdown of [3H]oleic acid-labelled phosphatidylcholine [( 3H]PC) to [3H]oleic acid and the enzymes of phospholipid base exchange (PLBE) by the incorporation of [14C]serine into membrane lipids. The activities of these enzymes in rat brain preparations were all increased by procedures which increase intracellular Ca2+, and were all inhibited to a varying extent by the presence of ethanol, 50 mM, in vitro. In contrast, the activities of PLA2 and PLBE enzymes were markedly increased in preparations from animals which had received ethanol chronically in vivo. Similarly, although the basal activity of PLC was only slightly increased in such preparations, depolarization induced the breakdown of a significantly greater fraction of radiolabelled PI than that which was obtained in control preparations. The results suggest compensatory alterations in the activity of Ca2+-activated enzymes of phospholipid metabolism in brain tissue during the continued presence of ethanol in vivo.

The dynamics of granular materials, particularly radial and axial segregation in horizontal rotating cylinders containing large and small particles, is studied by Magnetic Resonance Imaging (MRI). Stationary three-dimensional (3D) images and real-time two-dimensional (2D) structural images showing radial segregation, band formation, and band merging are reported. Quantitative local particle concentrations are measured in a noninvasive manner from the different magnetic resonance responses of the seeds throughout segregation. Data are acquired with sufficiently high temporal (300 ms for 2D images) and spatial resolutions (0.94 mm cubic voxels), to give insights into the underlying mechanisms of both radial and axial segregation. In particular, the increasing rate of the local particle concentration during radial segregation is quantified. Particle migration is observed in the bulk material of the 75% and 82% full cylinders during both radial and axial segregation, showing that this region beneath the avalanche layer does not behave as a solid body. We also provide direct experimental evidence to support recent numerical simulations of band merging.

Abstract— Chronic ethanol ingestion in rats leads to a slow rise in brain alcohol dehydrogenase activity which levels off after 2 weeks at approximately twice the initial activity. The half‐time of the rise is approximately 8 days. Abrupt withdrawal of the ethanol is followed by a rapid decline of the brain alcohol dehydrogenase activity to the normal level with a half‐time of approximately 15 h. The difference in time constants between the rise in enzyme activity during ethanol‐feeding and its decline following withdrawal suggests that the increased enzyme activity is at least in part the result of a reduced rate constant of enzyme degradation in the presence of ethanol. The effect of ethanol on brain alcohol dehydrogenase activity is not altered by supplementation of the diet with carbohydrate or vitamins. The effect is seen only in the cerebral hemispheres and not in the brain‐stem. Acquisition of tolerance to ethanol during chronic ethanol ingestion and its extinction following withdrawal follow almost the same time courses as the changes in brain alcohol dehydrogenase activity.

Long-term exposure to ethanol leads to an imbalance in different excitatory and inhibitory amino acids. When ethanol consumption is reduced or completely stopped, these imbalances in different amino acids and neurotransmitters are behaviorally expressed in the form of ethanol withdrawal. Glutamate, a major excitatory amino acid, and GABA, a major inhibitory amino acid, are responsible, at least partly, for ethanol withdrawal symptoms. The hypofunction of GABAA receptors and enhanced function of NMDA receptors are suggested to be responsible for the increase in the behavioral susceptibility during ethanol withdrawal. This imbalance between receptors may be exacerbated by repeated withdrawal. Because multiple and repeated periods of chronic ethanol consumption and withdrawal often occur in alcohol abusers, animal studies on the neurochemical changes in different amino acids following chronic ethanol treatment (CET) that is interrupted by repeated ethanol withdrawal episodes may be of clinical relevance for the development of treatment strategies. Brain glutamate increases during the first cycle of ethanol withdrawal, and this increase is much higher during the third cycle of ethanol withdrawal. The elevated glutamate released in the hippocampus during the first cycle of ethanol withdrawal episode was exacerbated in subsequent withdrawal episodes. Acamprosate, a drug used during human alcohol detoxification, is able to completely block the glutamate increase observed during the first as well as the third withdrawal of ethanol. In ethanol-naïve rats, there was no change in the glutamate microdialysate content after an acute ethanol injection. However, when repeated ethanol injections were cued with a vinegar stimulus that had previously been associated with the same ethanol injection, a significant increase in glutamate microdialysate content was assayed. Furthermore, when the cue was omitted, the ethanol injection induced no changes in glutamate microdialysate content in rats that had been previously ethanol conditioned. By comparison, a saline injection had no effect on extracellular glutamate concentration in rats naïve for ethanol as well as in rats daily administered with repeated ethanol injections that were not paired with the cue. It appears probable that these conditioned responses by extracellular glutamate concentrations may participate in the environmental cue-induced conditioned cravings for ethanol that are thought to be related to the high frequency of relapse in detoxified alcoholics.

Background:Hyperreactivity and impaired sensory gating of the acoustic startle response in alcohol dependence has been suggested to reflect a residual effect of previous detoxifications, increasing the severity of subsequent withdrawal episodes. Previous studies on the acoustic startle only included early‐onset alcohol‐dependent patients. The observed abnormalities may therefore also be specific for this subtype of alcohol dependence. We investigated the acoustic startle response in alcohol‐dependent patients and healthy controls and hypothesized that (i) early‐onset alcohol‐dependent patients show increased acoustic startle responses compared with late‐onset alcohol‐dependent patients and healthy controls, and (ii) the duration of alcohol dependence or the number of prior detoxifications would not explain the differences in the acoustic startle between early‐ and late‐onset alcohol dependence.Methods:The acoustic startle reflex was assessed in detoxified, male alcohol‐dependent patients (N = 83) and age‐matched healthy male controls (N = 86). Reflex eye blink responses to an auditory startle stimulus were measured by means of electromyographic recordings over the right orbicularis oculi muscle. Reflex amplitudes and levels of prepulse inhibition (PPI) were analyzed.Results:There was no association between number of previous withdrawals and the startle response or PPI. Early‐onset alcohol‐dependent patients showed higher acoustic startle amplitudes compared with late‐onset alcohol‐dependent patients and healthy controls [75/105 dB: F(2, 166) = 9.2, p < 0.001; 85/105 dB: F(2, 166) = 12.1, p < 0.001; 95 dB: F(2, 166) = 8.2, p < 0.001; 105 dB: F(2, 166) = 9.7, p < 0.001], and there were no differences in PPI.Conclusions:Increased acoustic startle response in detoxified early‐onset alcohol‐dependent patients may reflect a trait marker specifically involved in early‐onset alcohol dependence. The findings of the current study do not support the hypothesis that the increased startle response is a residual state marker.