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At least 19 recordsLinked to original sources

Pre-adaptation, adaptation and de-adaptation to high altitude in humans: cardio-ventilatory and haematological changes.

The aim of this study was first to investigate cardio-ventilatory and haematological responses induced by intermittent acclimation and second to study de-adaptation from high altitude observed after descent. To achieve these objectives nine subjects were submitted to intermittent acclimation in a low barometric chamber (8 h daily for 5 days, day 1 at 4500 m, day 5 at 8500 m) before an expedition to the Himalayas. Cardio-ventilatory changes were measured during a hypobaric poikilocapnic hypoxic test (4500 m, barometric pressure = 589 hPa) and haematological changes were studied at sea level. These measurements were performed before and after acclimation, after return to sea level, but also 1 and 2 months after the expedition. In addition, partial pressures of oxygen and carbon dioxide in arterial blood (PaO2, PaCO2) and arterial erythropoietin concentration [EPO] were measured at rest during the hypoxic test. Results suggested the pre-adaptation protocol was efficient since an increased PaO2 (+12%, P < 0.05), a smaller difference in alveolo-arterial PO2 ( -63%, P < 0.05) and a lower PaCO2 ( -11%, P < 0.05), subsequent to ventilatory changes, were observed after acclimation with a significant increase in reticulocytes and in sea level [EPO] (+44% and +62% respectively, P < 0.05). De-adaptation was characterized by a loss of these cardio-ventilatory changes 1 month after descent, whereas the haematological changes (increased red blood cells and packed cell volume, P < 0.05) persisted for 1 month before disappearing 2 months after descent. This study would also suggest that acute hypoxia performed after a sojourn at high altitude could induce significantly depressed EPO responses (P < 0.05).

Adaptation, Physiological↗

Cold-adapted variants of influenza A virus: evaluation in adult seronegative volunteers of A/Scotland/840/74 and A/Victoria/3/75 cold-adapted recombinants derived from the cold-adapted A/Ann Arbor/6/60 strain.

Influenza A/Scotland/74 (H3N2) and A/Victoria/75 (H3N2) cold-adapted (ca) recombinant viruses, prepared by mating the A/Ann Arbor/6/60 (H2N2) ca donor virus and influenza A wild-type virus, were evaluated in adult seronegative volunteers (serum hemagglutination-inhibiting antibody titer, </=1:8) for level of attenuation, antigenicity, and genetic stability of the temperature-sensitive and ca phenotypes. At 10(7.0) to 10(7.5) 50% tissue culture infective doses the A/Scotland/74 and A/Victoria/75 ca recombinant viruses were clearly attenuated and antigenic. However, one of eight vaccinees infected with 10(7.5) 50% tissue culture infective doses of the A/Scotland/74 ca recombinant had a febrile reaction (39 degrees C). At a 10-fold higher dose (10(8.5) 50% tissue culture infective doses), 4 of 12 A/Scotland/74 vaccinees had a febrile and/or systemic reaction. Febrile reactions were not observed in volunteers who received the A/Victoria/75 ca recombinant virus, whereas 3 of the 12 vaccinees had mild upper respiratory tract symptoms, in one instance associated with mild systemic manifestations. Significantly, the serum hemagglutination- and neuraminidase-inhibiting antibody responses were comparable to those induced by wild-type virus. Both ca recombinant viruses were shed in low titer for a short period of time. Each isolate retained the temperature-sensitive phenotype. However, there was evidence of genetic instability of the ca marker in that 7 of 24 isolates exhibited some loss of the ca property, and one isolate completely lost the capacity to produce plaques at 25 degrees C. The retention of a low level of residual reactogenicity in the A/Scotland/74 ca recombinant suggests that acquisition of the ca and temperature-sensitive phenotypes by a ca recombinant virus may not always bring about a satisfactory level of attenuation for individuals lacking hemagglutinin immunity.

Adaptation, Physiological↗

Adaptation to spatially heterogeneous modifying and adaptive environments.

The development of an individual's phenotype is influenced by environmental factors (the modifying environment) which may differ from those factors (the adaptive environment) that decide on the adaptational value of the developed phenotype. The shapes of adaptationally optimal norms of reaction are therefore essentially determined by associations between these two environmental components together with the degree of adaptational sensitivity of the developed phenotypes. Two complementary aspects of optimality are accounted for: (a) environments can be optimal for a given norm of reaction and (b) norms of reaction can be optimal for a given environment. The results are obtained for random distribution of genotypes over environmental conditions and under the physiologically reasonable premise that fitness is a function of the costs of modification and adaptation. It turned out that the associations of adaptive and modifying environments are the primary sources of adaptational optimization. More specifically, it is shown that (i) independence between the two environmental components constitutes an adaptationally optimal environment only for norms of reaction in which all phenotypes are adaptively insensitive; (ii) if costs of modification do not depend on the environment, and if the two environmental components are not associated, adaptationally optimal norms of reaction can always be realized through phenogenetic invariance; (iii) as a rule, adaptively sensitive phenotypes developed under strong environmental associations necessitate phenogenetic plasticity for the optimal norm of reaction; (iv) a norm of reaction which is adaptationally optimal in its adaptationally optimal environment can always be realized through phenogenetic invariance, if costs of modification do not vary with the environment. These results reveal an important role of patterns of adaptive sensitivity of phenotypes, which may even surpass that of shapes of norms of reaction in adaptational processes.

Adaptation, Physiological↗

Interactions between chromatic adaptation and contrast adaptation in color appearance.

Color appearance depends on adaptation processes that adjust sensitivity both to the average color in the stimulus (through light or chromatic adaptation) and to the variations in color (through contrast adaptation). We explored how these different forms of adaptation interact, by examining how the state of chromatic adaptation depends on the time-varying color contrasts in the stimulus, and conversely, how adaptation to the mean determines the stimulus contrasts underlying contrast adaptation. Light adaptation levels remain very similar whether observers adapt to a static chromaticity or to large temporal modulations in cone excitation that vary at rates of 0.5 Hz or higher. This suggests that up to the sites of light adaptation, the response to moderate contrasts is effectively linear and that the adaptation effectively averages over several seconds of the stimulus. For slower flicker rates color is differentially biased by the last half-cycle of the flicker, and perceived contrast may be altered by response polarization. This polarization selectively saturates responses to moderate (but not low) contrasts along the color direction complementary to the mean color bias, implying that the response changes occur within multiple mechanisms tuned to different chromatic axes. Chromatic adaptation often adjusts only partially to the mean color of the stimulus, and thus leaves a residual bias in the color appearance of the field. Contrast adaptation reduces perceived contrast relative to this residual color, and not relative to the stimulus that appears achromatic. Similarly, contrast discrimination thresholds appear lower around the residual color than around the achromatic point. Thus under biased states of chromatic adaptation alternative measures of 'zero contrast' can be dissociated, suggesting that they do not depend on a common null point within the channels encoding chromatic contrast.

Adaptation, Ocular↗

Contrast adaptation: paradoxical effects when the temporal frequencies of adaptation and test differ.

Previous studies of human contrast adaptation employing visually evoked potentials (VEP) have revealed contradictory results, namely, either a reduction or an enhancement in VEP amplitude. In a cross-adaptation experiment, we explored the possibility that differences in the temporal frequency of adapting and test patterns played a role. Phase-reversing checkerboard stimuli [1-deg check size, temporal frequency 8.5 or 17 reversals per second (rps)] served as adaptation and test pattern with contrasts of 0 or 97%. In 13 subjects, we recorded both retinal (PERG) and cortical (VEP) steady-state responses simultaneously. In a balanced block design, all four combinations of the temporal adaptation and test frequencies were employed. Contrast adaptation reduced the PERG amplitude by about 20% in every temporal condition (P < 0.001). The VEP amplitude was strongly affected by adaptation, but the effect differed in magnitude and sign depending on condition: With identical adaptation and test frequency, amplitude was reduced by 15% (P = 0.07) at 8.5 rps and by 38% at 17 rps (P < 0.05). Adapting at 8.5 rps and testing at 17 rps had a tiny (14%) insignificant effect, whereas adapting at 17 rps and testing at 8.5 rps revealed an amplitude enhancement of 27% (P < 0.05). These strong temporal cross-adaptation effects (in the VEP, but not in the PERG) suggest that the adaptable cortical mechanisms (gain control) can be narrowly tuned in their temporal properties. A sizable adaptation effect can even change its sign when varying the temporal frequency by a factor of two. This finding resolves contradictions between previous VEP adaptation studies and reconciles them with psychophysical findings.

Adaptation, Physiological↗

Perceived contrast following adaptation: the role of adapting stimulus visibility.

The issue of whether contrast adaptation can reduce the perceived contrast of gratings oriented orthogonal to the adapting stimulus to a greater extent than parallel gratings has been the subject of considerable debate (Snowden and Hammett, 1992; Ross and Speed, 1996). We compared the reductions in perceived contrast of various test gratings oriented parallel and orthogonal to the adapting stimulus across a range of spatial frequencies (2.25-9 c/deg) and adaptation contrasts (0.19-1.0). Our results show that when the adapting stimulus is low in contrast, parallel adaptation effects are always greater than the effects of orthogonal adaptation. When the adapting contrast is increased, however, the difference between parallel and orthogonal effects is reduced. Further increases in adapting contrast can produce a situation where cross-orientation adaptation effects exceed iso-orientation effects. This was observed at low spatial frequencies (2.25 and 4.5 c/deg) only. The difference in the pattern of results obtained at low and high spatial frequencies can be explained in terms of the adapting stimulus visibility. We conclude that cross-orientation adaptation effects can be greater than iso-orientation effects, but only when the adapting stimulus is highly suprathreshold.

Adaptation, Ocular↗

Distinct post-receptor alterations generate gene- and signal-selective adaptation and cross-adaptation of TLR4 and TLR2 in human leukocytes.

Gene- and signal-specific adaptation/tolerance of blood leukocytes to lipopolysaccharide endotoxin (LPS) occurs during human and animal septicemia. These phenotypes can be modeled in vitro. LPS-TLR4-adapted human THP-1 promonocytic cells cross-adapt to lipoteichoic acid (LTA)-TLR2-induced IL-1beta/TNF-alpha production, suggesting disruption of a common intracellular signaling event(s). A plausible explanation for homologous adaptation of TLR4 with heterologous adaptation of TLR2 is a persistent inactivation and degradation of IRAK1 following TLR4 activation. LTA stimulation of TLR2 also produces homologous adaptation of TLR2 with inactivation of IRAK1, but there is no detectable degradation of IRAK1. Strikingly, such LTA-adapted cells still respond to LPS stimulation of TLR4 with rapid activation and degradation of IRAK1, and robust IL-1beta/TNF-alpha production. Moreover, cells adapted to either LTA- or LPS-production of IL-1beta/TNF-alpha normally produce soluble interleukin 1 receptor antagonist (sIL-1Ra) anti-inflammatory protein when stimulated by either agonist. We conclude that: (i) disruption of a unique TLR2 signaling component upstream of IRAK1, but downstream of TLR2 sensing, induces homologous adaptation to LTA; (ii) disruption of IRAK1 may induce homologous adaptation of TLR4 to LPS and cross-adaptation of TLR2 to LTA; and (iii) TLR2/TLR4 signaling events that control sIL-1Ra translation do not adapt to LPS or LTA, indicating that TLR4 and TLR2 can still function. We present a hypothetical model of adaptation based on a signalsome, with IRAK1 evolving after IRAK4 to regulate TLR4 adaptation tightly.

Adaptation, Biological↗

Contrast adaptation in retinal and cortical evoked potentials: no adaptation to low spatial frequencies.

Contrast adaptation occurs in both the retina and the cortex. Defining its spatial dependence is crucial for understanding its potential roles. We thus asked to what degree contrast adaptation depends on spatial frequency, including cross-adaptation. Measuring the pattern electroretinogram (PERG) and the visual evoked potential (VEP) allowed separating retinal and cortical contributions. In ten subjects we recorded simultaneous PERGs and VEPs. Test stimuli were sinusoidal gratings of 98% contrast with spatial frequencies of 0.5 or 5.0 cpd, phase reversing at 17 reversals/s. Adaptation was controlled by prolonged presentation of these test stimuli or homogenous gray fields of the same luminance. When adaptation and test frequency were identical, we observed significant contrast adaptation only at 5 cpd: an amplitude reduction in the PERG (-22%) and VEP (-58%), and an effective reduction of latency in the PERG (-0.95 ms). When adapting at 5 cpd and testing at 0.5 cpd, the opposite effect was observed: enhancement of VEP amplitude by +26% and increase in effective PERG latency by + 1.35 ms. When adapting at 0.5 cpd and testing at 5 cpd, there was no significant amplitude change in PERG and VEP, but a small effective PERG latency increase of +0.65 ms. The 0.5-cpd channel was not adapted by spatial frequencies of 0.5 cpd. The adaptability of the 5-cpd channel may mediate improved detail recognition after prolonged blur. The existence of both adaptable and nonadaptable mechanisms in the retina allows for the possibility that by comparing the adaptational state of spatial-frequency channels the retina can discern between overall low contrast and defocus in emmetropization control.

Adaptation, Physiological↗

On the mechanism of adaptation to protein synthesis inhibitors by Tetrahymena. Facilitation, cross adaptation, and resensitization.

Tetrahymena is able to adapt to the presence of sublethal concentrations of many drugs which inhibit a wide variety of cellular functions. In spite of the generality of this phenomenon in Tetrahymena, the mechanism of adaptation at the cellular and molecular levels is unknown. This study deals mainly with adaptation to the protein synthesis inhibitors, cycloheximide and emetine. The physiological response of Tetrahymena to sublethal concentrations of these drugs is an immediate cessation of cell division for a period of time dependent on the drug concentration, followed by an abrupt resumption of exponential growth at a constant rate. By measuring the length of the growth lags under a variety of experimental conditions, we have confirmed several observations made by Frankel and coworkers, and provide evidence for two new phenomena associated with adaptation to cycloheximide: (a) adaptation to cycloheximide also results in adaptation of cells to emetine, another protein synthesis inhibitor not closely related structurally to cycloheximide. We have termed this phenomenon cross adaptation, (b) exposure to concentrations of cycloheximide too low to cause any growth lags or inhibition of protein synthesis significantly shortens the time required by cells to adapt to higher concentrations of cycloheximide. We have termed this phenomenon facilitation. Facilitation shows some degree of specificity in that facilitation with cycloheximide has no effect on adaptation to emetine. From this, we infer the existence of two distinct systems involved in adaptation to cycloheximide, one of which shows a higher degree of specificity towards cycloheximide than the other. We also show that transfer of adapted or facilitated cells to drug-free medium results in a gradual but complete resensitization. The kinetics of resensitization suggest that the cellular machinery responsible for adaptation and facilitation does not leave the cell, but is simply diluted out during cell division.

Adaptation, Physiological↗

Color perception under chromatic adaptation: red/green equilibria with adapted short-wavelength-sensitive cones.

Chromatic adaptation can dramatically alter the color appearance of a light. The specific effect of adapting short-wavelength-sensitive (SWS) cones is examined by using two adapting wavelengths that lie on a tritanopic confusion line. The change in color appearance caused by signals from adapted SWS cones is isolated by restricting the wavelengths of the test light to 550 nm or longer. Thus the test negligibly stimulates SWS cones, so their sensitivity does not affect the test's appearance. The results show that adapted SWS cones contribute redness to the appearance of a superimposed test light, while not affecting sensitivity of MWS and LWS cones. Quantitatively, the redness from SWS cones illuminated by a large adapting field approaches physical admixture of test and adapting lights. This is very different from an adapting field that stimulates only MWS and LWS cones which, due to a postreceptoral process, contributes much less redness to a small superimposed test than expected from admixture. The difference between the adapted SWS-cone and the adapted MWS/LWS-cone contributions to the color of a small test explains a surprising result: a bluish-green (491 nm) adapting field contributes redness to a superimposed test light.

Adaptation, Ocular↗

Short-chain fatty acids in the non-adapted and adapted pelvic ileal pouch.

BACKGROUND: Adaptation to colonic conditions occurs in the bacterial flora and faecal short-chain fatty acids (SCFAs) of the pelvic ileal pouch. METHODS: Faecal SCFAs were studied in 14 J-pouch patients within 10 days after closure of the ileostomy (non-adapted pouch) and more than 6 months after ileostomy closure (adapted pouch). RESULTS: Concentrations of faecal SCFAs were low in non-adapted pouches (mean +/- SE, 20.3 +/- 3.4 mmol/l), increasing to intermediate levels, 53.3 +/- 8.4 mmol/l, between 6 months and a year after ileostomy closure, and to 96.3 +/- 7.9 mmol/l, after more than a year of adaptation. Production of SCFAs in faecal homogenates was correspondingly low in non-adapted (6.3 +/- 2.0 mmol/l) compared with adapted pouches (32.0 +/- 3.6 mmol/l; p = 0.001) and could not be overcome by the addition of fermentable carbohydrates. Percentages of the predominant SCFAs (acetate, propionate, butyrate) were not affected by adaptation, nor were production and concentration of lactate. Stool volume decreased from 1019 +/- 134 to 603 +/- 77 ml/24 h (p = 0.02) during adaptation, sodium excretion decreased from 132 +/- 19 to 67 +/- 11 mmol/24 h (p = 0.02), and osmolality increased from 316 +/- 6 to 398 +/- 13 (p = 0.001). Excretions of carbohydrates, nitrogen, and potassium were not altered. CONCLUSIONS: The bacterial production of SCFAs is low in non-adapted pouches, resulting in low concentrations of SCFAs comparable to concentrations found in conventional ileostomies. Pouch adaptation gradually increases SCFA production and concentration severalfold and reaches concentrations normally found in non-colectomized individuals after approximately 1 year.

Adaptation, Physiological↗

Dual adaptation and adaptive generalization of the human vestibulo-ocular reflex.

In two experiments, we examined the possibility that the human vestibulo-ocular reflex (VOR) is subject to dual adaptation (the ability to adapt to a sensory rearrangement more rapidly and/or more completely after repeated experience with it) and adaptive generalization (the ability to adapt more readily to a novel sensory rearrangement as a result of prior dual adaptation training). In Experiment 1, the subjects actively turned the head during alternating exposure to a visual-vestibular rearrangement (target/head gain = 0.5) and the normal situation (target/head gain = 0.0). These conditions produced both adaptation and dual adaptation of the VOR but no evidence of adaptive generalization when tested with a target/head gain of 1.0. Experiment 2, in which exposure to the 0.5 gain entailed externally controlled (i.e., passive) whole body rotation, resulted in VOR adaptation but no dual adaptation. As in Experiment 1, no evidence of adaptive generalization was found.

Adaptation, Physiological↗

[Adaptation to stress can enhance animal resistance to sublethal hypoxia to a greater extent than adaptation to hypoxia].

Wistar male rats were adapted to intermittent hypoxia in an altitude chamber (group 1) and to short-term immobilization stress (group 2). The animals of both series and control ones were exposed to severe hypoxic hypoxia in acute experiment: they were anesthetized and inhaled a gas mixture which contained 6% O2. In the first two hours of the experiment the death rate was 65% in control, 10% in adaptation to stress, and 29% in adaptation to hypoxia. Principal parameters of respiration, circulation, and basic-acid equilibrium were monitored during the experiment. They allowed us to establish that both the variants of adaptation increased the tissue oxygen consumption; furthermore, adaptation to hypoxia preserved a higher level of oxygen consumption than adaptation to stress. Despite this, in adaptation to stress the death rate was threefold higher than in adaptation to hypoxia. This result was explained by the accumulation of heat shock proteins in cells during adaptation to stress and the resultant development of a phenomenon of adaptive stabilization of structures (PhASS). In adaptation to hypoxia the PhASS did not develop.

Acute Disease↗

Pyrithiamine adaptation of Staphylococcus aureus. I. Adaptation and carbohydrate utilization.

Das, S. K. (University of Calcutta, Calcutta, India) and G. C. Chatterjee. Pyrithiamine adaptation of Staphylococcus aureus. I. Adaptation and carbohydrate utilization. J. Bacteriol. 83:1251-1259. 1962.-Staphylococcus aureus has been adapted to pyrithiamine, a thiamine analogue; as a result of this adaptation, the color of the pigment of the organism changes from orange-yellow to lemon-yellow. The adaptation is reversible; the adapted strain will revert after repeated subculture in a medium containing thiamine and no pyrithiamine. Of the major biochemical alterations resulting from adaptation, severe depression in glucose utilization and simultaneous stimulation of acetate utilization have been noticed. The effect of metabolic inhibitors on the utilization of glucose and acetate has also been studied. By measuring the rate of formation of C(14)O(2) from glucose-1-C(14) and glucose-6-C(14), it has been observed that the reduction in C(14)O(2) formation from glucose-1-C(14) by the adapted organism is much more than that obtained from glucose-6-C(14), causing thereby a decreased metabolic ratio of these two substrates after such adaptation. Relative to the normal strain, the adapted strain utilizes acetate-C(14) at a much faster rate, both in the formation of C(14)O(2) and also in the incorporation of C(14) into the protein and lipid fractions; the rate of formation of C(14)O(2) from pyruvate-1-C(14) is not greatly altered. It has been postulated that there is a partial blocking of the pentose phosphate cycle, because of the lowered glucose-1-C(14) utilization, and simultaneous stimulation of the tricarboxylic acid cycle; or perhaps the initiation of some other route after pyrithiamine adaptation would account for the great increase in acetate utilization.

Acclimatization↗

Does cortical motion adaptation exhibit functional properties analogous to light adaptation in the retina?

PURPOSE: The retina codes variations in luminance by adapting to and hence discounting, the mean luminance. During adaptation to a moving pattern, perceived speed decreases. Thus we know that the adapted visual system does not simply code the absolute speed of a stimulus. We hypothesize that adaptation to a moving stimulus serves to optimize coding of changes in speed at the expense of maintaining an accurate representation of absolute speed. In this case we would expect discrimination of speeds around the adapted level to be preserved or enhanced by motion adaptation. METHODS AND RESULTS: After adaptation to motion in the same direction as a subsequent test stimulus, seven of eight subjects showed a reduction of perceived speed in the adapted region and seven showed enhanced discrimination. CONCLUSIONS: We conclude that motion adaptation preserves or enhances differential speed sensitivity at the expense of an accurate representation of absolute speed in a manner analogous to retinal light adaptation.

Adaptation, Ocular↗

Membrane current noise in dark-adapted and light-adapted isolated retinal rods of the larval tiger salamander.

1. Low-frequency light-sensitive membrane current noise in isolated rod photoreceptors of the larval tiger salamander was recorded using suction electrodes, in the dark, and during light adaptation by backgrounds or by bleaching visual pigment. 2. In background light, noise variance increases and then decreases. For rods desensitized to similar levels by bleaching visual pigment, the noise variance either does not change (weak adaptation) or decreases (with stronger adaptation). 3. The power spectral density of the current noise in dark-adapted rods shows a component with half-power cut-off frequency at about 0.1 Hz, attributed to spontaneous single events and continuous noise from dark phosphodiesterase activity. A second component, with half-power cut-off frequency at about 1 Hz, may be due to slow components in the light-sensitive channel gating. 4. The power spectral density of the noise in background light is dominated by noise generated by the background. Background light adapts at least the first component of the noise seen in dark-adapted cells. For cells desensitized by bleaching, light adaptation of both components of the dark-adapted noise is observed. 5. The results confirm that the low-frequency noise in dark-adapted cells arises from the transduction mechanism of the rod, in that both components can be light adapted, and show that, for rods permanently desensitized by bleaching, the desensitization is not due to the presence of active visual pigment molecules similar to those produced by background light.

Adaptation, Ocular↗

Effect of localized grating adaptation as a function of separation along the length axis between test and adaptation areas.

Aftereffect following adaptation to localized gratings was measured as a function of the separation along the length axis between test and adaptation gratings. When the adaptation gratings were located on or near the retinal area occupied by the test grating, contrast sensitivity greatly decreased. When the adaptation gratings were spatially separated from the test grating, contrast sensitivity significantly increased. This property is similar to that which was observed in our previous study, in which the adaptation gratings were displaced from a test grating along the modulation axis. The facilitatory aftereffect of the grating adaptation can be accounted for by assuming that there may exist two mechanisms involved in the adaptation process; one is a center mechanism responsible for the detection of a test pattern, its adaptation producing a reduction in responsiveness; the other is a surround mechanism which tonically inhibits the center mechanism, its adaptation resulting in an increase in the sensitivity of the center mechanism by releasing the tonic inhibition. The spatial property of the adaptation effect may reflect the nature of spatial integration process of the center and surround mechanism.

Adaptation, Ocular↗