Objective and Subjective Time Courses of Recovery from Motion Sickness Assessed by Repeated Motion Challenges

1997 ◽  
Vol 7 (6) ◽  
pp. 421-428
Author(s):  
J.F. Golding ◽  
J.R.R. Stott
Keyword(s):  
Motion Sickness ◽  
Time Course ◽  
Rotational Velocity ◽  
Head Movements ◽  
Time Interval ◽  
Subjective Time ◽  
Loss Of Tolerance ◽  
Time Courses ◽  
Subsequent Motion ◽  
Moderate Nausea

The aim of this study was to determine whether the time course of recovery of tolerance, as assessed objectively by rechallenge with motion, paralleled the subjective recovery from motion sickness. Subjects (n = 20) were exposed to 5 pairs of nauseogenic motion challenges in which the time interval between the end of the first and the start of the second of each pair ranged from 15 min to 2 h. The cross-coupled motion challenge had an incrementing profile of rotational velocity from 4° to 92°.s-1 in steps of 4°.s-1 every 30 s, with 8 head movements per 30 s, of approximately 45°, and was continued to the point of moderate nausea. Objective loss of tolerance decreased from 15 min to 60 min after the first challenge, but increased again at 2 h. By contrast, most individuals reported subjective recovery by 15 min to 30 min. It was concluded that there is an underlying effect of motion sickness that sensitizes the response to subsequent motion for a period of at least 2 h. This underlying objective effect can occur in the absence of subjective symptoms, has a slower time course than the subjective recovery from symptoms and appears to be non-monotonic.

Kinetics of ammonia production and excretion in the acidotic dog

1965 ◽  
Vol 209 (6) ◽  
pp. 1206-1212 ◽  
Author(s):  
Georges Fulgraff ◽  
Robert F. Pitts
Keyword(s):  
Renal Artery ◽  
Time Course ◽  
Time Interval ◽  
Ammonia Production ◽  
Rapid Injection ◽  
Collecting Ducts ◽  
Distal Tubules ◽  
Time Courses ◽  
Rate Limiting ◽  
Kinetics Of

The Chinard technique of rapid injection into one renal artery of a glomerular marker (creatinine) and a compound whose utilization or excretion is under investigation has been employed in a study of the time courses of production and excretion of ammonia. Following the injection of N15H4 Cl or amide-N15-labeled glutamine, the label appeared in the urinary ammonia within a partially corrected time interval of 11 sec or less, suggesting that, in both instances, the labeled ammonia entered the urine as far along the nephron as the convoluted portion of distal tubules and cortical collecting ducts. Creatinine appeared in the urine after a delay of 60–100 sec. Following injections of amino-N15-labeled glutamine, appearance of label in urinary ammonia was delayed about 20 sec relative to that observed following injection of amide-N15-labeled glutamine. The time course of disappearance of label from the urine suggests that deamidation of glutamine is not rate-limiting for ammonia production and excretion, whereas deamination of glutamine may well be.

Dichotomy in perceptual learning of interval timing: calibration of mean accuracy and precision differ in specificity and time course

2013 ◽  
Vol 109 (2) ◽  
pp. 344-362 ◽  
Author(s):  
Hansem Sohn ◽  
Sang-Hun Lee
Keyword(s):  
Perceptual Learning ◽  
Time Course ◽  
Temporal Dynamics ◽  
Interval Timing ◽  
Time Interval ◽  
Psychophysical Experiment ◽  
Subjective Time ◽  
Sensory Stimuli ◽  
Accuracy And Precision ◽  
Observer Model

Our brain is inexorably confronted with a dynamic environment in which it has to fine-tune spatiotemporal representations of incoming sensory stimuli and commit to a decision accordingly. Among those representations needing constant calibration is interval timing, which plays a pivotal role in various cognitive and motor tasks. To investigate how perceived time interval is adjusted by experience, we conducted a human psychophysical experiment using an implicit interval-timing task in which observers responded to an invisible bar drifting at a constant speed. We tracked daily changes in distributions of response times for a range of physical time intervals over multiple days of training with two major types of timing performance, mean accuracy and precision. We found a decoupled dynamics of mean accuracy and precision in terms of their time course and specificity of perceptual learning. Mean accuracy showed feedback-driven instantaneous calibration evidenced by a partial transfer around the time interval trained with feedback, while timing precision exhibited a long-term slow improvement with no evident specificity. We found that a Bayesian observer model, in which a subjective time interval is determined jointly by a prior and likelihood function for timing, captures the dissociative temporal dynamics of the two types of timing measures simultaneously. Finally, the model suggested that the width of the prior, not the likelihoods, gradually shrinks over sessions, substantiating the important role of prior knowledge in perceptual learning of interval timing.

Inducing Cortical Plasticity to Manipulate and Consolidate Subjective Time Interval Production

2021 ◽  
Author(s):  
Motoyasu Honma ◽  
Shoko Saito ◽  
Takeshi Atsumi ◽  
Shin‐ichi Tokushige ◽  
Satomi Inomata‐Terada ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Time Interval ◽  
Subjective Time ◽  
Interval Production

scholarly journals Pseudo-streaming potentials in Necturus gallbladder epithelium. II. The mechanism is a junctional diffusion potential.

1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton
Keyword(s):  
Time Course ◽  
Bathing Solution ◽  
Intercellular Spaces ◽  
Similar Time ◽  
Streaming Potentials ◽  
Osmotic Water ◽  
Lateral Intercellular Spaces ◽  
Transepithelial Voltage ◽  
Time Courses ◽  
Good Agreement

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.

scholarly journals Sodium and calcium currents in dispersed mammalian septal neurons.

1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Calcium Currents ◽  
Closing Time ◽  
Patch Clamp Technique ◽  
Average Value ◽  
Time To Peak ◽  
Time Courses ◽  
Fast Activation ◽  
Septal Neurons

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.

scholarly journals Mechanisms of autoantibody production in autoimmune MRL mice.

1980 ◽  
Vol 152 (5) ◽  
pp. 1302-1310 ◽  
Author(s):  
D S Pisetsky ◽  
G A McCarty ◽  
D V Peters
Keyword(s):  
Antibody Response ◽  
Time Course ◽  
Fundamental Difference ◽  
Autoantibody Production ◽  
Quantitative Expression ◽  
Autoantibody Response ◽  
Time Courses ◽  
Antibody Levels

The quantitative expression of anti-DNA and anti-Sm antibodies has been investigated in autoimmune MRL-lpr/lpr and MRL-+/+ mice. Anti-Sm antibodies were detected in sera from 21/23 lpr/lpr and 10/16 +/+ mice, with individual animals showing striking variation in the time-course and magnitude of this autoantibody response. The peak antibody levels of the responding animals of each substrain did not differ significantly. For anti-DNA antibody, a different pattern of responsiveness was observed. Individual animals of each substrain produced very similar responses in terms of the magnitude and time-course of serum anti-DNA antibody. The differences in the peak levels of the two substrains were highly significant, with lpr/lpr mice demonstrating a much greater anti-DNA antibody response than +/+ mice. In lpr/lpr mice tested for both autoantibody systems, serum anti-DNA and anti-Sm antibodies showed distinct time-courses. These studies indicate that anti-DNA and anti-Sm antibodies are expressed independently in MRL mice, with the expression of anti-DNA, but not anti-Sm antibody markedly influenced by the presence of the 1pr gene. A fundamental difference in the mechanisms involved in the generation of anti-DNA and anti-Sm antibodies is suggested by the quantitative pattern of the two responses.

“Torso Rotation”' experiments. 4: the role of vision and the cervico-ocular reflex in compensation for a deficient VOR

1999 ◽  
Vol 9 (2) ◽  
pp. 89-101
Author(s):  
L.J.G. Bouyer ◽  
D.G.D. Watt
Keyword(s):  
Motion Sickness ◽  
Vestibular Function ◽  
Repeated Exposure ◽  
Head Movements ◽  
Upper Body ◽  
Calibration Data ◽  
En Bloc ◽  
Mean Velocity ◽  
Gaze Stability ◽  
Velocity Gain

Acute, reversible changes in human vestibular function can be produced by exposure to “Torso Rotation” (TR), a method involving the overuse of certain types of simple, self-generated movements. A single session results in multiple, short-lasting aftereffects, including perceptual illusions, VOR gain reduction,gaze and postural instability, and motion sickness. With repeated exposure, motion sickness susceptibility disappears and gaze stability improves. VOR gain continues to be reduced, however. Therefore, another gaze stabilizing system must come into play. Are visual and/or neck inputs involved in this functional compensation? Six subjects participated in this 7-day experiment. Eye and head movements were measured during 2 tests: 1) voluntary “head only” shaking between 0.3 and 3.0 Hz (lights off) and 2) voluntary “head and torso” shaking, moving the upper body en bloc (neck immobilized). Measurements were obtained before and repeatedly after TR. Velocity gain (eye velocity/head velocity) was determined for each of these tests. Each day, mean velocity gain during “head only” shaking in the dark (averaged over 1.0 to 2.0 Hz) dropped significantly after TR ( P < 0.01), with no long-term improvement ( P > 0.9). Similar results, although more noisy, were obtained for “head and torso” shaking. As a control, EOG calibration data confirmed that gaze stability in the light did improve over the 7 days of testing. This experiment demonstrates that the reduction in gaze instability following repeated exposure to TR results from an increased use of vision. It excludes the VOR, the COR, and predictive mechanisms (including efference copy) as contributors. In addition, in the 20 minutes following TR completion, gaze stability recovered less than during previous VOR testing in the dark. These results are compatible with the motion that exposure to TR leads to a change in sensorimotor strategy involving a de-emphasis of vestibular inputs.

scholarly journals The atypical cation-conduction and gating properties of ELIC underscore the marked functional versatility of the pentameric ligand-gated ion-channel fold

2015 ◽  
Vol 146 (1) ◽  
pp. 15-36 ◽  
Author(s):  
Giovanni Gonzalez-Gutierrez ◽  
Claudio Grosman
Keyword(s):  
Quaternary Ammonium ◽  
Time Course ◽  
Three Dimensional ◽  
Mouse Muscle ◽  
Current Decay ◽  
Quaternary Ammonium Cations ◽  
Inward Currents ◽  
Time Courses ◽  
Extracellular Side ◽  
Invariant Functional

The superfamily of pentameric ligand-gated ion channels (pLGICs) is unique among ionotropic receptors in that the same overall structure has evolved to generate multiple members with different combinations of agonist specificities and permeant-ion charge selectivities. However, aside from these differences, pLGICs have been typically regarded as having several invariant functional properties. These include pore blockade by extracellular quaternary-ammonium cations in the micromolar-to-millimolar concentration range (in the case of the cation-selective members), and a gain-of-function phenotype, which manifests as a slower deactivation time course, as a result of mutations that reduce the hydrophobicity of the transmembrane pore lining. Here, we tested this notion on three distantly related cation-selective members of the pLGIC superfamily: the mouse muscle nicotinic acetylcholine receptor (nAChR), and the bacterial GLIC and ELIC channels. Remarkably, we found that, whereas low millimolar concentrations of TMA+ and TEA+ block the nAChR and GLIC, neither of these two quaternary-ammonium cations blocks ELIC at such concentrations; instead, both carry measurable inward currents when present as the only cations on the extracellular side. Also, we found that, whereas lidocaine binding speeds up the current-decay time courses of the nAChR and GLIC in the presence of saturating concentrations of agonists, the binding of lidocaine to ELIC slows this time course down. Furthermore, whereas mutations that reduce the hydrophobicity of the side chains at position 9′ of the M2 α-helices greatly slowed the deactivation time course of the nAChR and GLIC, these mutations had little effect—or even sped up deactivation—when engineered in ELIC. Our data indicate that caution should be exercised when generalizing results obtained with ELIC to the rest of the pLGICs, but more intriguingly, they hint at the possibility that ELIC is a representative of a novel branch of the superfamily with markedly divergent pore properties despite a well-conserved three-dimensional architecture.

scholarly journals Dynamic Change in Cells Expressing IL-1β in Rat Hippocampus after Status Epilepticus

2014 ◽  
Vol 5 ◽  
pp. JCM.S13738 ◽  
Author(s):  
Satoru Sakuma ◽  
Daisuke Tokuhara ◽  
Hiroshi Otsubo ◽  
Tsunekazu Yamano ◽  
Haruo Shintaku
Keyword(s):  
Status Epilepticus ◽  
Cellular Localization ◽  
Wistar Rats ◽  
Time Course ◽  
Dynamic Change ◽  
Chronic Phase ◽  
Pyramidal Cells ◽  
Reactive Astrocytes ◽  
Time Courses ◽  
Ca3 Pyramidal Cells

Background The time course of cytokine dynamics after seizure remains controversial. Here we evaluated the changes in the levels and sites of interleukin (IL)-1β expression over time in the hippocampus after seizure. Methods Status epilepticus (SE) was induced in adult Wistar rats by means of intraperitoneal injection of kainic acid (KA). Subsequently, the time courses of cellular localization and IL-1β concentration in the hippocampus were evaluated by means of immunohistochemical and quantitative assays. Results On day 1 after SE, CA3 pyramidal cells showed degeneration and increased IL-1β expression. In the chronic phase (>7 days after SE), glial fibrillary acidic protein (GFAP)–-positive reactive astrocytes–-appeared in CA1 and became IL-1β immunoreactive. Their IL-1β immunoreactivity increased in proportion to the progressive hypertrophy of astrocytes that led to gliosis. Quantitative analysis showed that hippocampal IL-1β concentration progressively increased during the acute and chronic phases. Conclusion IL-1β affects the hippocampus after SE. In the acute phase, the main cells expressing IL-1β were CA3 pyramidal cells. In the chronic phase, the main cells expressing IL-1β were reactive astrocytes in CA1.

scholarly journals Changes in blood hemoglobin and blood gases PaO2 and PaCO2 in severe COPD over a three-year telemonitored program of long-term oxygen treatment

2012 ◽  
Vol 7 ◽  
Author(s):  
Roberto W. Dal Negro ◽  
Silvia Tognella ◽  
Luca Bonadiman ◽  
Paola Turco
Keyword(s):  
Time Course ◽  
Blood Gases ◽  
Wilcoxon Test ◽  
Background Information ◽  
First Year ◽  
Oxygen Treatment ◽  
Blood Hemoglobin ◽  
Time Courses ◽  
Severe Copd

Background: Information on the effects of long-term oxygen treatment (LTOT) on blood hemoglobin (Hb) in severe COPD are limited. The aim was to assess blood Hb values in severe COPD, and investigate the time-course of both Hb and blood gas changes during a 3-year telemetric LTOT. Methods: A cohort of 132 severe COPD patients (94 males; 71.4 years ± 8.8 sd), newly admitted to the tele-LTOT program, was investigated. Subjects were divided according to their original blood Hb: group A: <13 g/dL; group B: ≥13<15 g/dL; group C: ≥ 5<16 g/dL; group D: ≥16 g/dL. Blood Hb (g/dL), PaO2 and PaCO2 (mmHg), SaO2 (%), and BMI were measured at LTOT admission (t0), and at least quarterly over three years (t1-t3). Wilcoxon test was used to compare t0 vs. t1 values; linear regression to assess a possible Hb-BMI relationship; ANOVA to compare changes in Hb time-courses over the 3 years. Results: LTOT induced a systematic increase of PaO2, and changes were significant since the first year (from 52.1 mmHg± 6.6sd to 65.1 mmHg± 8.7 sd, p<0.001). Changes in SaO2 were quite similar. Comparable and equally significant trends were seen in all subgroups (p<0.001). PaCO2 dropped within the first year of LTOT (from 49.4 mmHg± 9.1sd to 45.9 mmHg ±7.5 sd, p<0.001): the t0-t1 comparison proved significant (p<0.01) only in subgroups with the highest basal Hb, who showed a further PaCO2 decline over the remaining two years (p<0.001). Hb tended to normalization during LTOT only in subgroups with basal Hb>15 g/dl (ANOVA p<0.001); anemic subjects (Hb<13 g/dl) ameliorated not significantly in the same period (ANOVA = 0.5). Survival was independent of the original blood Hb. Anemia and polyglobulia are differently prevalent in COPD, the latter being the most represented in our cohort. LTOT affected both conditions, but to a different extent and according to different time-courses. The most striking Hb improvement was in polyglobulic patients in whom also PaO2, PaCO2 and SaO2 dramatically improved. In anemic subjects effects were smaller and slower, oxygenation being equally ameliorated by LTOT. Conclusions: LTOT effects on Hb and PaCO2 are regulated by an Hb-dependent gradient which seems independent of the original impairment of blood gases and of effects on oxygenation.

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