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PubMed1977

[Injury from the deceleration and acceleration of human skulls (author's transl)].

Diametral injuries of the skull accidental force may be accepted as an effect of summation of osseous and cerebral oscillations which cause a gradient of pressure inside the skull. The cavitations of liquor between cerebrum and skull are of no influence neither in a positive nor a negative direction in transmission of the vibration. Situated in an area which is not effected by the oscillation the hypophysis is protected against trauma. The causes for the contre-coup is to be seen in the anatomical and morphological specificity of the skull following Newton's axioms. Several concepts of the contra-coup are discussed.

Acceleration↗
PubMedDate not supplied

Posterior avulsion of the optic nerve due to deceleration trauma.

A patient with complete transection of the optic nerve (posterior avulsion) and explosion of the eyeball, due to an attempted suicide is reported. The symptoms, mechanism of injury and therapeutic possibilities in complete transection and in partial posterior optic nerve avulsions are discussed. Although this case ended up with enucleation, the partial avulsions are not without hope. The importance of team-work is emphasized in polytraumatic patients.

Deceleration↗
PubMed2000

Hydrogen peroxide decelerates recovery of action potential after high-frequency fatigue in skeletal muscle.

Effects of reactive oxygen species (ROS), especially hydrogen peroxide (H(2)O(2)), on recovery of action potential by resting for 30 min after high-frequency fatigue were studied using frog skeletal muscle fibers. After stimulation at a frequency of 50 HZ for 2 min, the action potential amplitude was decreased by 14.5 mV from controls, and resting membrane was depolarized by 15.4 mV. Action potential duration was also prolonged by high-frequency stimulation (1.5 ms in controls to 2.6 ms). The high-frequency stimulation used here caused no muscle damage. The action potential was partially improved after a 30-min rest. Addition of catalase at 500 units/ml or H(2)O(2) at 0.5 mM to sartorius muscle did not alter any of the parameters of the action potential after high-frequency stimulation. Treatment with catalase accelerated post-fatigue recovery of the action potential. Application of H(2)O(2) delayed post-fatigue recovery of resting and action potentials. When added to detubulated toe muscle fibers, catalase no longer improved the attenuation of action potential induced by high-frequency stimulation, even after a 30-min rest. These findings suggest that removal of H(2)O(2) from transverse tubules is effective for post-fatigue recovery of action potential in skeletal muscle.

Action Potentials↗
PubMed1998

Apoptosis rate can be accelerated or decelerated by overexpression or reduction of the level of elongation factor-1 alpha.

Peptide chain elongation factor-1 alpha (EF-1 alpha) is required for the binding of aminoacyl-tRNAs to acceptor sites of ribosomes during protein synthesis. More recently, EF-1 alpha has been shown to be involved in cytoskeletal organization. The elongation factor functions in actin bundling and microtubule severing. Moreover, it can activate the phosphatidylinositol-4 kinase whose substrates are involved in regulation of actin polymerization. The expression level of EF-1 alpha is regulated in many situations such as growth arrest, transformation, and aging. Because of this regulation of EF-1 alpha in various states of cell life, and its key position in protein synthesis as well as cytoskeletal organization, we chose to investigate the effect of its expression levels on apoptosis. Apoptosis is a complex event regulated through numerous activators and inhibitors. In some situations, protein synthesis is required for apoptosis to be triggered. Investigation of the effect of altered levels of elongation factor-1 alpha on apoptosis is of particular interest since it may affect both protein synthesis and cytoskeletal organization. For example, reduction of EF-1 alpha leads to a reduced protein synthesis rate, which might reduce the presence of those "killer factors" triggering apoptosis. EF-1 alpha involvement in cytoskeletal organization is another example, since cytoskeletal organization undergoes dramatic changes during apoptosis. Thus, this study has been planned to ascertain whether hypo- and hyperexpression of EF-1 alpha protein, achieved by constructing expression vectors with the EF-1 alpha cDNA in its antisense or sense orientation under the control of a cytomegalovirus promoter, can produce stable transfectants with either heightened or reduced responsiveness to apoptosis stimuli. Our results show the following: (1) induction of apoptosis by serum deprivation shows that antisense EF-1 alpha provides cells significant protection from apoptotic cell death and (2) EF-1 alpha overexpression causes a faster rate of cell death. These findings suggest that when EF-1 alpha protein is abundant the cells are proapoptosis, and vice versa in low abundance the cells are in the mode of antiapoptosis. Therefore, changes in levels of EF-1 alpha may be one of the global pivotal regulators modulating the rate of apoptosis.

3T3 Cells↗
PubMed1996

Sustained increase in rat myocardial alpha 1A-adrenoceptors induced by 6-hydroxydopamine treatment involves a decelerated receptor turnover.

The biochemical mechanisms involved in the alpha 1-adrenoceptor up-regulation and possible changes in subtypes of adrenoceptors in the rat heart after chemical denervation were investigated. The effects of acute 6-hydroxydopamine treatment (two increasing doses 24 h apart) on the pseudo-steady state densities and turnover rates of alpha 1-adrenoceptors were studied in ventricular myocardium of the rat. We have assessed the repopulation kinetics of [3H]prazosin binding sites after irreversible inactivation of alpha 1-adrenoceptors induced by a single dose of phenoxybenzamine (1 mg/kg i.p.) in rats acutely treated either with 6-hydroxy-dopamine or with vehicle (control animals). Seven days after the last administration of 6-hydroxydopamine an enhanced density of [3H]prazosin binding sites (Bmax 58.7 +/- 3.6 fmol/mg protein vehicle-treated rats versus 82.6 +/- 5.3 fmol/mg protein 6-hydroxydopamine-treated rats) was observed. This was not accompanied by changes in the dissociation constant value. Furthermore, the proportion of high affinity sites for WB-4101 was altered (21 +/- 2% versus 72 +/- 3% for animals treated with vehicle and 6-hydroxydopamine, respectively). In rat myocardium, alpha 1-adrenoceptor turnover, evaluated during the 6-hydroxydopamine-induced up-regulation (7-19 days after the completion of treatment with 6-hydroxydopamine) revealed an increase in the half-life of the alpha 1-adrenoceptor (t1/2 of 67.2 h versus 38.7 h in control animals). The present study confirms an increase in alpha 1-adrenoceptors in rat myocardium after chemical denervation and reveals that the effect is almost completely confined to the alpha 1A-adrenoceptor subtype. Furthermore, the up-regulation of alpha 1A-adrenoceptors is the result of a decrease in the cellular processes that control the rate of receptor degradation.

Adrenergic Agents↗
PubMed1980

The production and generalization of large-magnitude heart rate deceleration by contingently faded biofeedback.

Eight subjects were taught to decrease their heart rates via biofeedback training. Four of these received contingently faded, beat-by-beat analogue feedback and contingent reinforcement each time their performance met a specified and adjusting criterion. The other four received continuous, beat-by-beat analogue feedback, but not the contingent reinforcement. Subjects in the two groups were yoked to ensure equal densities of reinforcement. Subjects in the first group were asked to decrease heart rates 15% from baseline and were then trained using only 75%, 50% and 25% of beat-by-beat feedback. It was hypothesized that the immediate reinforcement of appropriate behavior and the contingent fading (following mastery) of feedback would aid in the generalization of the response. Following completion of all criterion steps or 10 training sessions, whichever came first, all subjects were tested with no feedback and no contingent reinforcement. The group receiving contingently faded feedback training showed a significantly greater heart rate decrease in the training sessions and also the test session. These results were interpreted as indicating that biofeedback can be conceptualized as an operant conditioning paradigm, and that the use of operant techniques may help subjects produce clinically significant changes.

Biofeedback, Psychology↗