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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From the accordance of the discharge and recruitment behaviour of motor units with the Fourier-analysis of the tremor ripples it is shown that the action tremor originates from any muscle innervation and is equivalent to the mechanical effect of the discharges of all motoneurones of a particular muscle. The power spectrum of tremor is mainly caused by the twitch contractions between recruitment (7--8/sec) and total fusion (25/sec) of the discharging motoneurones. The maximum of the frequency spectrum, which represents the dominant tremor rate, corresponds to the discharge frequency just after recruitment of each motoneurone. The twitch contractions of these newly recruited motor units are mechanically least fused. The power spectrum of the tremor in patients with motor disturbaces parallels the changes in the discharge and recruitment behaviour of motoneurones during voluntary contraction. The correlation between the discharges of two simultaneously recorded motor units shows a tendency to synchronization of all discharge rates the extent of which corresponds to the individual tremor intensity.
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PMID:[Tremor. Mechanical effect of the discharge behavior of motor neurons]. 62 Sep 83

To examine the secretory production of heterologous proteins by Streptomyces lividans, we fused the DNA encoding the signal peptide of the alpha-amylase inhibitor tendamistat, derived from S. tendae with a synthetic gene encoding the thrombin inhibitor hirudin. The analysis of secretion by immunoblots revealed an efficient translocation of hirudin through the membrane, with no detectable immunoreaction among the cellular proteins. The secreted hirudin was stable in the shaking culture for about 6 days. A comparison of the hirudin secreted by S. lividans and recombinant reference hirudin from yeast by immunoblots and thrombin inhibition assays shows that hirudin from Streptomyces has a lower specific activity, which may be due to a different aminoterminal sequence or to inexact processing of the precursor.
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PMID:Synthesis and secretion of hirudin by Streptomyces lividans. 136 34

The clinical and physiological features of six new patients with primary orthostatic tremor are described. We suggest that use of the term primary orthostatic tremor be confined to the clinical syndrome in which unsteadiness when standing is the predominant complaint and accompanied by characteristic electrophysiological findings of a rapid (frequency around 16 Hz), regular leg tremor which is not influenced by peripheral feedback, is synchronous between homologous leg muscles, and in certain postures of the upper limbs, between muscles of the arm and leg. The fast frequency of muscle activity in primary orthostatic tremor of the legs causes unsteadiness when standing (presumably due to partially fused muscle contraction) but only a fine ripple of muscle activity is visible. In contrast, the slower frequency of other leg tremors, for example essential tremor, results in obvious leg movement which is evident in many leg postures, is variable over time and can be reset by a peripheral nerve stimulus. Essential tremor and orthostatic tremor do not respond to the same therapies, suggesting differences in the pharmacological profiles of the two conditions. Accordingly, there are clinical, physiological and pharmacological differences between primary orthostatic and essential tremor. Whether these factors are sufficient to regard these tremors as separate conditions is discussed.
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PMID:Primary orthostatic tremor: further observations in six cases. 159 87

Several mouse mutations cause unstable locomotion, tremor, seizures, and a reduced lifespan because of deficient myelin formation in the central nervous system. Mutant alleles at the shiverer (shi) locus are the only ones in this series with a selective molecular defect, namely, in myelin basic proteins (MBPs), which are virtually absent in shi homozygotes and 50% reduced in heterozygotes. In the present study, backcross and intercross matings indicate recombination of 21.2 +/- 3.3% between myelin deficient, shimld, and fused phalanges, syfp, a marker near the middle of chromosome 18. Recombination of shimld with twirler (Tw), a marker near the centromere, is 45.7 +/- 4.9%. Thus, the shi locus maps near the distal end of mouse chromosome 18 and is the first available marker for this region. Given the evidence of other workers that an MBP locus maps to the same mouse chromosome, and that part of this chromosome may be syntenic with an MBP-PEPA region on human chromosome 18, it is likely that shi is in or near an MBP gene.
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PMID:Shiverer gene maps near the distal end of chromosome 18 in the house mouse. 241 73

PATIENTS WITH TREMOR OF PARKINSONISM SHOW THREE CHARACTERISTICS OF MOTOR UNIT ACTIVITY: rhythmic spontaneous resting discharge, abnormally low firing rates during voluntary contraction, and consistent differences in firing pattern between small and large motor units. Smaller units discharge once per tremor beat at weak contractions but change into bursts of two or three spikes per beat at stronger forces. Large units are later recruited and fire preferentially once per beat. The large tremor amplitudes can be partly explained by synchronization of unfused twitches of low frequency units which summate more powerfully than the partially fused contractions during physiological tremor, which is about twice as rapid. Tremor is strongly influenced by the force of voluntary contraction. It is strongest at rest or during weak muscular effort and with increasing force becomes continuously of higher frequency and smaller amplitude. Both changes are the consequence of increasing discharge rates of motoneurones at stronger contractions.
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PMID:Correlation between tremor, voluntary contraction, and firing pattern of motor units in Parkinson's disease. 441 18

Soluble plasma inducers and inhibitors of platelet activity and fluid dynamics of the blood stream are effective modulators of platelet-vessel wall interactions. Effects of platelet activity inducers, arachidonic acid (AA) and stable prostaglandin endoperoxides analogue (U46619), on platelet disposition on the bottom of multiwell tissue culture plates coated with fibrillar calf skin collagen (CSC) have been studied by scanning electron microscopy (SEM). Both agents stimulate platelet spreading and formation of large surface-bound multilayer (thrombi-like) aggregates on a CSC substrate. AA and U46619 effects on spreading and thrombi-like aggregate formation depend on the speed of platelet suspension shaking during platelet deposition on the surface. In the absence of shaking, both inducers mainly stimulate the spreading of platelets: spread platelets fuse and form widespread sheets covering up to 50% of the CSC-coated surface. An increase in the shaking speed leads to the decrease of the platelet spreading, while the number of surface-bound thrombi-like aggregates grows, reaching the maximum at a shaking speed of 40 back and forth cycles per min. The thrombi-like aggregates mainly consist of fused platelets and always contain the basal sheet of spread platelets, which suggests the participation of the latter in aggregate attachment to the surface. Large aggregates are absent in the population of nonadherent platelets. The obtained data indicate that AA metabolites participate in platelet spreading and thrombi-like aggregate formation, the processes specific for platelet-surface interactions. The use of the suggested model for the in vitro study of platelet spreading and mural thrombi formation, and for screening of antithrombotic and thrombolytic drugs is discussed.
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PMID:Arachidonic acid and stable analogue of prostaglandin endoperoxides (U46619) induce platelet spreading and thrombi-like aggregate formation on a collagen substrate. Effect of fluid dynamics. 641 75

Manipulation of the single conventional myosin heavy chain (mhc) gene in Dictyostelium discoideum (Dd) has delineated an essential role for the filament-forming, or light meromyosin (LMM) domain of the myosin molecule in cytokinesis, development, and in the capping of cell surface receptors (see Spudich: Cell Regulation 1:1-11, 1989; Egelhoff et al.: Journal of Cell Biology, 112:677-688, 1991a). In order to assess the functional relationship between sarcomeric and cytoplasmic myosins, a chimeric gene encoding the Dd myosin head and subfragment 2 fused to rat beta cardiac LMM was transfected into both wild-type and Dd mhc null cells. Chimeric myosin was organized into dense cortical patches in the cytoplasm of both wild-type and Dd mhc null cells. Although null cells expressing chimeric mhc at approximately 10% of Dd mhc levels were unable to grow in shaking suspension or to complete development, chimeric myosin was able to rescue capping of cell surface receptors, to associate with filamentous actin, and to localize to the correct subcellular position during aggregation. Deletion of 29 amino acids in the rod corresponding to a previously defined filament assembly competent region eliminated the cortical patches and the posterior localization during chemotaxis. Taken together, these observations suggest that sarcomeric and cytoplasmic myosin rods are functionally interchangeable in several aspects of nonmuscle motility.
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PMID:Functional analysis of a cardiac myosin rod in Dictyostelium discoideum. 806 39

1. The triceps surae (TS) stretch reflex was measured in decerebrate cats during crossed extensor stimulation and after spinalization during rhythmic locomotor activity induced by clonidine and manual perineal stimulation. The TS force in response to sinusoidal stretch was measured at a given contraction level before and after deafferentation, and the 'reflex force' was computed by subtracting these two responses. Reflex 'gain' was computed as the ratio of the reflex and deafferented force responses (a unitless estimate of the open loop feedback gain). 2. Prior to locomotion the spontaneous muscle activity was low (less than 15% of maximum), but the reflex gain was relatively high (close to 1.0 with a 5 Hz stretch). When locomotion commenced the reflex gain was markedly lowered when measured at the same contraction level as before locomotion (25% of the gain prior to locomotion). At higher contraction levels the reflex gain was not significantly increased. The reflex force and EMG responses to stretch increased with the contraction level, but their effect on the total reflex gain was cancelled by an associated increase in the intrinsic muscle stiffness. 3. In the decerebrate cat, during weak tonic contractions (spontaneous), the reflex gain was high and comparable with the gain in the resting spinal cat. However, with increased tonic contractions produced by crossed extensor stimulation the reflex gain dropped. At higher contraction levels the gain was not significantly different from the gain during spinal locomotion. 4. When the frequency of stretch was increased from 3 to 20 Hz, EMG responses to stretch increased, but the reflex force decreased, since a more fused contraction developed with the more frequent reflex activations. Overall, the reflex gain decreased with frequency in both spinal and decerebrate cats. The phase lag of the reflex force, relative to the intrinsic muscle force, increased with increasing frequency, due to reflex delays, with a 180 deg lag occurring between 12 and 18 Hz (tremor frequencies). The mean gain was significantly lower and the phase lag was significantly greater during locomotion than during tonic crossed extensor contractions, suggesting different reflex mechanisms. 5. In conclusion, during locomotion in spinal cats afferent feedback from low frequency ankle movements, similar to those occurring during the normal step cycle, reflexly produces a small but significant fraction of the extensor force (about a quarter of the stretch-related force modulation). This fraction is remarkably constant at the different contraction levels of the step cycle. Afferent feedback during higher frequency movement is less effective, minimizing the chance of instability and tremor. In contrast during tonic contractions afferent feedback produces half of the total muscle force during perturbations, clearly contributing to the maintenance of posture.
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PMID:Gain of the triceps surae stretch reflex in decerebrate and spinal cats during postural and locomotor activities. 893 Aug 48

Cucurbita maxima trypsin inhibitor I (CMTI-I), a member of the squash-type protease inhibitor family, is composed of 29 amino acids and shows strong inhibition of trypsin by its compact structure. To study the structure-function relationship of this inhibitor using protein engineering methods, we constructed an expression system for CMTI-I as a fused protein with porcine adenylate kinase (ADK). A Met residue was introduced into the junction of ADK and CMTI-I to cleave the fusion protein with CNBr, whereas a Met at position 8 of authentic CMTI-I was replaced by Leu. Escherichia coli JM109 transformed with the constructed plasmid expressed the fused protein as an inclusion body. After cleavage of the expressed protein with CNBr, fully reduced species of CMTI-I were purified by reversed-phase HPLC and then oxidized with air by shaking. For efficient refolding of CMTI-I, we used 50 mM NH4HCO3 (pH 7.8) containing 0.1% PEG 6000 at higher protein concentration. Strong inhibitory activity toward trypsin was detected only in the first of three HPLC peaks. The inhibitor constant of CMTI-I thus obtained, in which Met8 was replaced by Leu, was 1.4 x 10(-10) M. The effect of replacement of Met with Leu at position 8 was shown to be small by comparison of the inhibitor constant of authentic CMTI-III bearing Lys at position 9 (8.9 x 10(-11) M) with that of its mutant bearing Leu at position 8 and Lys at position 9 (1.8 x 10(-10) M). To investigate the role of the well conserved hydrophobic residues of CMTI-I in its interaction with trypsin, CMTI-I mutants in which one or all of the four hydrophobic residues were replaced by Ala were prepared. The inhibitor constants of these mutants indicated that those with single replacements were 5-40 times less effective as trypsin inhibitors and that the quadruple mutant was approximately 450 times less effective, suggesting that the hydrophobic residues in CMTI-I contribute to its tight binding with trypsin. However, each mutant was not converted to a temporary inhibitor.
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PMID:Synthesis of a squash-type protease inhibitor by gene engineering and effects of replacements of conserved hydrophobic amino acid residues on its inhibitory activity. 901 Sep 39

The aim of this study was to see whether action tremor contributes to the weakness which can be measured in some muscles in patients with Parkinson's disease, by preventing fully fused contraction of motor units. Strength and action tremor were recorded during maximal wrist extension in patients when they were on and off antiparkinsonian medication, and in age- and sex-matched healthy subjects. Peak torque and mean rectified EMG levels were reduced by 25% and 30% (n = 7), respectively, when patients were off medication (compared with when they were on medication). In parkinsonian patients off treatment, action tremor was visible in torque and EMG records, and had a frequency of approximately 10 Hz. The absolute amplitude of this tremor was considerably smaller in patients on medication and in control subjects. In patients, medication reduced action tremor in torque and EMG by 37% and 57%, respectively, so that tremor amplitude approached that in normals. Similar changes were seen when action tremor was expressed as % peak torque of % mean rectified EMG. In parkinsonian patients off medication, a 10-Hz synchronizing influence dominates muscle activity at the wrist. The results is an incompletely fused muscle contraction, which is an important factor contributing to the weakness present in the off-medication state. Antiparkinsonian medication releases motor units from the 10-Hz synchronizing influence, enabling higher discharge rates, fused contraction and improved force generation.
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PMID:Does parkinsonian action tremor contribute to muscle weakness in Parkinson's disease? 912 52


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