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PubMed1987

Abnormal expression of surface immunoglobulin isotypes on antigen-binding B lymphocytes from mice tolerant to trinitrophenyl determinants.

Temporary B-cell tolerance to the trinitrophenyl (TNP) hapten can be produced in BDF1 mice by intraperitoneal injection of trinitrobenzene sulfonic acid (TNBS). Antigen-binding cells (ABC) specific to TNP, measured as TNP donkey erythrocyte rosettes, are found in tolerant mice as well as in immune mice. We have studied the surface immunoglobulin isotype profile of these TNP-binding lymphocytes (TNP-ABC) in four groups of animals: nonimmune, immune, tolerant, and tolerant-challenged. Immune mice received intravenous TNP sheep erythrocytes (TNP-SRC), whereas tolerant-challenged mice received TNP-SRC and TNBS on Day 0. TNP-ABC from mice immunized with TNP-SRC exhibit increased expression of surface IgG and decreased expression of surface IgD, compared to the ABC from nonimmune mice. Tolerant mice have a higher proportion of ABC with surface IgG, and a lower proportion with surface IgD, than nonimmune mice. Tolerant-challenged mice have a lower proportion of ABC with surface IgG, and a higher proportion with surface IgD, than immune mice. Thus, B-cell tolerance in this model entails an attenuation of the surface immunoglobulin isotype switch (loss of IgD and gain of IgG) on ABC seen in the normal immune response. For most TNP-ABC, tolerogen exposure prevents the switch in surface isotypes normally induced by exposure to TNP antigen; i.e., the tolerance lesion precedes the surface isotype switch. However, a minority of the TNP-ABC appear to switch surface isotypes in response to the tolerogen itself.

Animals↗
PubMed1991

Soluble factors in tolerance and contact sensitivity to DNFB in mice. X. IL-2 is the activation signal mediating release of synthesized suppressor factor.

Two signals are required for the in vitro activation of Lyt2+ T suppressor cells (Ts) from mice tolerized with 2,4-dinitrobenzene sulfonate (DNBS) to produce soluble suppressor factors (SSF) which suppress the transfer of contact sensitivity to dinitrofluorobenzene (DNFB). Recognition of DNP/class I MHC (signal one) stimulates the Ts to synthesize SSF. Release of SSF requires a soluble mediator (signal two) produced by the interaction of L3T4+ T cells from tolerant mice with I-A on metabolically functional cells in the DNP-presenting cell population. The purpose of this study was to examine the nature of this second Ts activation signal. Coculture of tolerant spleen cells and glutaraldehyde-fixed (Glu-) DNP-labeled spleen cells (DNP-SC) resulted in the synthesis but not release of SSF. Addition of either IL-1 or IL-2 to these cultures induced SSF release. Treatment of such cultured cells with the anti-murine IL-2 receptor antibody PC 61.5.3 blocked the IL-2- and IL-1-stimulated release of SSF. Release of SSF was also blocked when tolerant cells were cultured with (unfixed) DNP-SC in the presence of a monoclonal anti-IL-2 antibody. IL-2 but not IL-1 was able to stimulate the Ts to release synthesized SSF in the absence of L3T4+ TH activity. First, addition of IL-2 to cocultures of tolerant cells and DNP-presenting I-A- cells induced release of the synthesized SSF, whereas addition of IL-1 did not. Second, IL-2 also stimulated SSF release in cocultures of L3T4+ T cell-depleted tolerant cells and Glu-DNP-SC, whereas IL-1 did not. Tolerant cells pretreated with IL-2 and then washed were able to synthesize and release SSF upon culture with Glu-DNP-SC. Pretreatment of tolerant cells with IL-1 did not stimulate SSF release upon subsequent culture with Glu-DNP-SC. These results indicate that the Lyt2+ Ts from DNBS-tolerant mice express IL-2 receptors and IL-2 is the lymphokine which induces the Ts to release synthesized SSF. Thus, IL-2 provides a differentiative signal during the functional activation of these regulatory T cells.

Animals↗
PubMedDate not supplied

A method for the rapid development of opiate tolerance in the guinea pig ileum.

The rate and degree of in vitro tolerance development to morphine, normorphine and d,1-methadone were assessed on the excised guinea pig ileum. Agonists in fixed concentrations at 1/4, 1/2, 1 and 2 x IC50 were incubated with the tissue for 1, 2 or 4 hours. The degree of tolerance development was expressed as a ratio of the IC50 after and before incubation. A high degree of tolerance developed to all three agonists and the effect could be prevented by co-incubation with naloxone. Tolerance development was stereo-specific; levorphanol and 1-methadone developed much higher degrees of tolerance than their respective d-isomers. Furthermore, under the same conditions, subsensitivity to acetylcholine, norepinephrine, and adenosine monophosphate did not develop. The in vitro tolerance was accompanied by physical dependence development as evidenced by the fact that naloxone elicited muscular contracture in the tolerant ileum. cAMP enhanced the development of tolerance to normorphine and cycloheximide could reduce this phenomenon. It is concluded that the procedure may facilitate studies on the mechanisms involved in the development of opiate tolerance and physical dependence.

Animals↗
PubMed1992

Tolerance to the anticonvulsant effects of clobazam in mice.

Tolerance to the anticonvulsant effects of clobazam has been studied in three murine models of epilepsy: pentylenetetrazole- and N-methyl-D,L-aspartic acid-induced seizures and audiogenic-induced seizures in the DBA/2 strain. Tolerance occurred most rapidly in the pentylenetetrazole model but the development of tolerance could be reduced by increasing the dose interval. Tolerance to the protective effects of clobazam occurred more readily to the first tonic seizure than to the full tonic clonic seizure. The development of tolerance could not be attributed to smaller concentrations of clobazam in brain or to increasing concentrations of the metabolite. Although slower to develop, tolerance to clobazam did occur in the N-methyl-D,L-aspartate model. However, tolerance to the protection from the full tonic clonic seizure in DBA/2 mice could not be detected, even when the dose of clobazam was reduced to the smallest dose that acutely protected most of the mice. In contrast, the protection given by clobazam to the induction of the wild-run in DBA/2 mice, did exhibit tolerance. Studies on the mechanism of tolerance to the anticonvulsant activity of benzodiazepines must take account of the seizure model used and the dose and interval between doses.

Acoustic Stimulation↗
PubMed1986

Influence of ambient temperature on the development and maintenance of tolerance to ethanol-induced hypothermia.

The development of tolerance to the hypothermic effect of ethanol was examined during chronic ethanol treatment (5 g/kg PO daily) at various ambient temperatures (Ta). Tolerance to the hypothermic effect of ethanol, monitored at five-day intervals for 25 days, developed rapidly when ethanol treatment was carried out at 4 degrees C. On the other hand, rats receiving ethanol treatment at a Ta of 36 degrees C, at which they did not experience hypothermia, acquired tolerance more slowly, but achieved the same level of tolerance as other groups after 25 days of treatment. This cannot be accounted for by the repeated testing at 21 degrees C at five-day intervals, since it was also observed under a non-repeated testing condition. Once tolerance to the hypothermic effect of ethanol was acquired, termination of ethanol treatment resulted in the loss of tolerance, but mere prevention of the hypothermic effect of ethanol did not. These results suggest that tolerance still developed even though the organisms did not experience hypothermia during ethanol treatment. Therefore there appears to be a component of tolerance, that depends upon a direct cellular action of the drug, as distinct from the physiological consequences of that action. However, variation in the degree of physiological disturbance (hypothermia) during drug exposure can modulate the rate of development of this tolerance.

Adaptation, Physiological↗
PubMed1988

Effect of chronic pentobarbital treatment on the development of cross-tolerance to ethanol and barbital.

Recently, we reported that a chronic regimen of ethanol by intubation, which produced clear tolerance to ethanol-induced hypothermia, ataxia and sleep, produced only a marginal degree of cross-tolerance to these effects of pentobarbital. The present experiments were designed to test the reverse process by examining cross-tolerance to pentobarbital after chronic pretreatment with ethanol, chronic pentobarbital treatment by gavage conferred clear cross-tolerance to both barbital- and ethanol-induced hypothermia, ataxia and sleep. In a separate experiment, cross-tolerance to barbital- and ethanol-induced hypothermia and ataxia was demonstrated over a wide range of test doses. Determination of ethanol blood levels as well as a complete time course of absorption, distribution and elimination of ethanol suggested that pharmacokinetic alterations may play a role in the development of cross-tolerance to ethanol in pentobarbital-treated subjects. The asymmetry of cross-tolerance raises the possibility that pentobarbital and ethanol invoke tolerance by mechanisms that are not wholly identical. This possibility requires further exploration. Conceivably the actions of ethanol which mediate the measured effects form a subset of a larger range of pentobarbital actions that could provide a stronger stimulus to tolerance development.

Animals↗
PubMed1991

Onset of tolerance to discriminative stimulus effects of morphine.

Experiments assessed the onset of tolerance to discriminative stimulus effects of morphine in rats treated repeatedly with twice daily doses of 10 mg/kg morphine. Saline and 3.2 mg/kg morphine were established as discriminative stimuli for food-reinforced fixed-ratio performances in several groups of rats, and initial ED50 values were determined for stimulus and rate-altering effects of morphine. To assess onset of tolerance, training was halted and 10 mg/kg doses of morphine were administered repeatedly at 12-h intervals. In separate experiments, ED50 values were redetermined after various treatment periods. One treatment with 10 mg/kg morphine did not alter the ED50 for stimulus effects of morphine, whereas treatment for one or three days increased the ED50 by approximately 2-fold. Comparisons with published data showed even greater tolerance when treatment lasted one or two weeks. Tolerance to stimulus effects of morphine generally was accompanied by tolerance to its rate-decreasing effects. Repeated treatment with morphine also produced cross-tolerance to morphine-like stimulus effects of methadone and buprenorphine. As with morphine itself, greater tolerance developed with longer treatment. These results suggest that tolerance to discriminative stimulus effects of morphine develops gradually, with magnitude of tolerance increasing as a function of treatment duration.

Animals↗
PubMedDate not supplied

Differential expression of benzodiazepine anticonvulsant cross-tolerance according to time following flurazepam or diazepam treatment.

In previous studies in which the anti-pentylenetetrazol (PTZ) effect of benzodiazepines was used to measure tolerance, the results depended on the benzodiazepine used for chronic treatment as well as the benzodiazepine given acutely to test for tolerance. In this study, the time course of tolerance reversal was studied in rats given two treatments known to cause anticonvulsant tolerance, 1-week flurazepam (FZP), and 3-week diazepam (DZP). Neither treatment altered convulsive threshold for IV PTZ, but both treatments decreased the convulsive threshold for bicuculline. Withdrawing DZP, but not FZP, treatment resulted in a loss of body weight. Twelve hours after 1-week FZP treatment, all benzodiazepines were significantly less effective, showing tolerance. Forty-eight hours after the 1-week FZP treatment, tolerance was still observed with DZP, FZP, and zolpidem, but was no longer present with clonazepam or bretazenil. After the 3-week DZP treatment, rats were tolerant to all benzodiazepines tested at 12 h of withdrawal, but had lost tolerance to all the drugs except bretazenil by 48 h. The results suggest differences in the way these benzodiazepines interact with their receptors, allowing differential expression of tolerance, and that chronic DZP and FZP treatments affected interactions of the benzodiazepines with their receptors, but not in the same fashion.

Animals↗
PubMed1981

The effect of cyclic nucleotides on tolerance induction by dinitrophenyl-isologous immunoglobulin G.

When tolerance to a hapten is induced by injecting the hapten conjugated to isologous immunoglobulin (Ig) G (dinitrophenyl (DNP)-IgG), the hapten remains on the surface of the antigen binding cell (ABC) for the duration of the tolerant state. Although this has been interpreted as a receptor blockade of ABC, it does not necessarily indicate that physical blocking of antigen receptors is the only mechanism of tolerance. Data are presented which suggest that cyclic nucleotides play a role in the in vitro induction of tolerance by DNP-IgG. Agents that elevate intracellular cyclic adenosine 3',5' monophosphate (cAMP) levels were added to lymphocytes during tolerance induction in vitro by DNP-IgG. Dibutyryl cAMP, theophylline, aminophylline, and isobutyl alpha-methylxanthine were able to inhibit the induction of tolerance to DNP. On the other hand, addition of dibutyryl cyclic guanosine 3',5'-monophosphate (cGMP) to lymphocytes incubated with doses of DNP-IgG that ordinarily are too low to induce tolerance facilitated tolerance induction. The possible role of these intracellular second messengers in the induction to tolerance is discussed.

Aminophylline↗
PubMed1986

Nitrate tolerance.

Nitrates are widely used in anginal prophylaxis. In spite of the fact that the concept of nitrate tolerance was first put forward many years ago, the question of tolerance has remained controversial. There is widespread agreement that tolerance does occur to the effects of nitrates on arterial pressure. In contrast, tolerance to the venous and pulmonary effects is disputed. Similarly, the possibility of tolerance to the antianginal effects remains at issue. In this review, I discuss the factors which may have contributed to conflicting results in different studies, in particular recent findings on the rapidity of onset and reversal of tolerance. Tolerance develops rapidly on initiation of treatment and disappears equally rapidly on its discontinuation. In addition, tolerance appears to be a function of plasma nitrate profile. It is most likely to occur when plasma nitrate levels are constant and least likely when nitrate levels fluctuate. Furthermore, the provision of a daily nitrate free interval may protect against the development of tolerance. I then discuss the implications of these findings for patient management. They suggest that nitrate prophylaxis should not be used continuously, if this can be avoided. Rather, prophylaxis should be tailored to the individual to provide protection at times of maximum susceptibility, while allowing nitrate levels to fall at other times. The adequacy of antianginal protection with drug regimens incorporating a nitrate free interval requires further assessment. Similarly, the possibility that a nitrate free interval might lead to withdrawal effects and exacerbation of angina needs to be excluded.

Angina Pectoris↗
PubMed1985

Cross-tolerance between dermorphin and morphine to analgesia and catalepsy in rats.

Rats were made tolerant to dermorphin or to morphine by continuous ICV infusion of these drugs. Tolerance to the analgesic effect was assessed by evaluating the shift of the ED50 of dermorphin or morphine in dermorphin-infused or in morphine-infused animal respectively, after single doses of these opioids. Tolerance to catalepsy was revealed with the significant reduction of this effect after single ICV dose of morphine in morphine-infused and dermorphin in dermorphin-infused rats. Both dermorphin and morphine induced tolerance to the analgesic and cataleptic effects. Acute administration (SC and ICV) of morphine in DER-tolerant rats induced a significant decrease of the analgesic and cataleptic effects of this opioid, showing the onset of cross-tolerance between morphine and dermorphin. Acute injections of dermorphin (ICV) in MOR-tolerant rats, while significantly decreasing its analgesic potency, indicating the development of cross-tolerance, did not modify the cataleptic response to the peptide, showing that no cross-tolerance was present to this effect.

Analgesia↗
PubMed1994

Effect of morphine tolerance and abstinence on the binding of [3H]naltrexone to discrete brain regions and spinal cord of the rat.

1. The effect of morphine tolerance and abstinence on the binding of [3H]naltrexone to discrete brain regions and spinal cord of the rat was determined. 2. Male Sprague-Dawley rats were implanted s.c. under light ether anesthesia with six morphine pellets for a 7-day period. Each pellet contained 75 mg of morphine base. Rats implanted with six placebo pellets each served as controls. 3. This procedure resulted in the development of tolerance to morphine as evidenced by decreased analgesic response to various doses of morphine. 4. The binding characteristics (Bmax or Kd values) of [3H]naltrexone, an opiate receptor antagonist, were determined in various tissues of morphine tolerant and abstinent rats. In the tolerant rats, the pellets were left in place at the time of sacrificing, whereas in the abstinent rats, the pellets were removed 18 hr prior to sacrificing. 5. The binding of [3H]naltrexone to opiate receptors on membranes prepared from brain regions (hypothalamus, hippocampus, cortex, pons and medulla, midbrain, corpus striatum and amygdala) and spinal cord of rats from various treatment groups was determined. 6. [3H]Naltrexone bound to tissue membranes at a single high affinity binding sites. The Bmax values of [3H]naltrexone to bind to opiate receptors on the membranes of amygdala and striatum were increased significantly in morphine tolerant rats when compared to the placebo controls, but the Kd values did not differ. 7. The Bmax and Kd values of [3H]naltrexone did not differ in any other brain region or spinal cord of morphine tolerant rats and their placebo controls. The binding constants of [3H]naltrexone were unaffected in morphine abstinent rats. 8. Previously we had shown that the binding of [3H]D-Ala2, MePhe4, Gly-ol5 enkephalin (DAMGO), a highly specific agonist for mu-opiate receptors was decreased in cortex, pons and medulla and spinal cord of morphine tolerant but not in the abstinent rats. In addition, delta and kappa receptors are unaffected in morphine tolerant and abstinent rats. 9. The results suggest that direction of change, as well as, the brain areas for mu-agonist and -antagonist opiate binding sites are affected differentially in morphine tolerant rats.

Analgesics↗
PubMedDate not supplied

Effect of 3-amino-1,2,4-triazole on the hypothermic effect of ethanol and on ethanol tolerance development.

The effect of aminotriazole (AT), inhibitor of catalase activity, on hypothermia and narcosis induced by ethanol and on the acquisition of tolerance to the ethanol hypothermic and narcotic effect was studied. Rats were pretreated with AT (1 g/kg IP) 1 hour before the test dose of ethanol (2.76 g/kg IP) and narcosis time, hypothermia and ethanol blood levels evaluated (first test). For studies on tolerance to ethanol, rats of the first test received daily (for 7 days) a dose of AT (1 g/kg IP) 1 hour before ethanol (2.76 g/kg) given by gavage, and the same parameters evaluated (8th day test). Results were compared to similar groups of rats without AT pretreatment (controls, 1st and 8th day test). Rats pretreated with AT exhibited a shorter narcosis time induced by ethanol but this treatment did not alter the hypothermic effect of ethanol nor ethanol disposal rate. Chronic ethanol treatment induced tolerance to the narcotic and hypothermic effect of ethanol as well as a metabolic tolerance. AT administered daily before the dose of ethanol produced a partial blockade of the development of tolerance to the narcotic effect of ethanol, but did not alter the development of hypothermic or metabolic tolerance. The brain catalase system seems to play a role in narcosis and on the development of tolerance to this effect of ethanol, but not in the hypothermic effect or in the development of tolerance to this ethanol effect. Since the inhibition of liver catalase activity by AT treatment was not correlated with changes in ethanol disposal rate, the liver catalase system appears not to play a role in the metabolic tolerance.

Amitrole↗
PubMedDate not supplied

Chronic intragastric infusion produces tolerance to ethanol in LS and SS mice.

Tolerance to ethanol's effects is seen after chronic injections and after chronic treatment with ethanol-containing liquid diets. However, tolerance associated with injections is often associated with environmental cuing (learned tolerance) and liquid diets do not allow for careful control of dose. The studies reported here demonstrate that chronic (3 g/kg every 6 h for 7 days) intragastric infusion of ethanol produces tolerance to ethanol in both LS and SS mice, as measured by sleep time and effects on open field activity and body temperature. LS mice developed more tolerance for all measures than the SS. The rate of ethanol elimination was increased slightly in both the LS and SS mouse lines following chronic ethanol infusion, which suggests that both lines developed a modest metabolic tolerance to ethanol. In contrast, the waking blood ethanol levels were altered only in the LS mice, which argues that some of the tolerance to ethanol seen in the LS mice is pharmacodynamic tolerance. Thus, chronic intragastric infusion of ethanol is a reliable method for treating animals chronically with ethanol that allows for the precise control of dose and dose interval, oral administration of ethanol, and minimal animal handling that can be associated with drug delivery, thereby reducing the risk of developing learned tolerance to ethanol.

Animals↗
PubMed1987

Conditioned tolerance to drug-induced (poly I:C) natural killer cell activation: effects of drug-dosage and context-specificity parameters.

Three experiments were conducted to evaluate the role of drug-dosage and stimulus-specificity parameters on the tolerance of drug-induced (poly I:C) natural killer (NK) cell activity. In the first experiment a protocol which provided mice with four weekly 20 micrograms/mouse ip injections of the immunostimulatory synthetic polynucleotide (poly I:C) following exposure to either a simple odor cue or a complex cue resulted in tolerance of NK cell activity. The identical protocol with a higher drug dose (50 micrograms/mouse) did not produce tolerance. In a second experiment, the stimulus specificity of tolerance was assessed by giving two groups of mice repeated signaled drug injections. For one of these groups the final poly I:C injection of the series was signaled, while for the other group it was not. Although both groups were tolerant relative to controls not previously exposed to the drug, indirect evidence of conditioning was obtained. Specifically, it was found that tolerance among mice receiving the signal on the test was such that they were not different from undrugged controls, while uncued mice had significantly higher levels of NK cell activity. The third experiment evaluated the role of stimulus specificity within an extinction paradigm. It was found that tolerance was reversed in mice provided with repeated nonreinforced reexposure to drug-signaling cues, while mice exposed to novel cues remained tolerant. These results further support the hypothesis that associative factors contribute to the tolerance of a drug-induced immune response.

Animals↗
PubMed1992

Repeated anticonvulsant testing: contingent tolerance to diazepam and clobazam in kindled rats.

The acute anticonvulsant efficacy of diazepam (1.5 mg/kg, i.p.) was evaluated by repeated test injection in kindled rats subcutaneously implanted with diazepam-filled or empty silastic tubes for 3 weeks. Tolerance developed to acute test injections in both diazepam- and sham-implanted rats. Tolerance developed to a lesser extent in another group of diazepam-implanted rats which did not receive acute intermittent anticonvulsant tests. The hypothesis that contingent tolerance had developed to the anticonvulsant actions of benzodiazepines (diazepam, 1.5 mg/kg, i.p. and clobazam, 10 mg/kg, i.p.) in kindled rats given acute intermittent injections was investigated using a 'before-after' design. Significant contingent tolerance developed in rats which received intermittent benzodiazepine treatment before, but not after, amygdala stimulation. Tolerance developed to different extents depending on the seizure measure evaluated (forelimb clonus duration, amygdala afterdischarge duration, motor seizure latency and duration, and seizure stage). Contingent tolerance to both benzodiazepines developed at a similar rate. The findings suggest that contingent tolerance may contribute a sizeable component to the overall functional benzodiazepine tolerance measured in long-term anticonvulsant drug studies in kindled rats. Several questions regarding contingent tolerance phenomena are posed and the implications of these findings for studies using repeated anticonvulsant testing are discussed.

Animals↗
PubMed1993

A system for testing the development and reversal of anticonvulsant tolerance to benzodiazepines in mice.

Tolerance to the anticonvulsant effects of benzodiazepines limits their use in epilepsy treatment. Animal models producing tolerance have been developed, but they require repetitive injections over several days or use silastic capsules which must be made for each drug and do not provide a constant infusion rate. Alzet 2001 osmotic pumps deliver at a constant rate (1 microliter/h) and dosage can be easily adjusted. Various solvents, PEG 400, propylene glycol, 2% Tween, 50% DMSO, saline, Molecusol, and 0.5% methyl cellulose, were tried and found unsuitable because benzodiazepines were not maintained in solution or proconvulsant activity was seen. Tetraglycol was chosen as it did not demonstrate these shortcomings. Anticonvulsant activity was evaluated by PTZ i.v. tail infusion using forelimb clonus as the endpoint. This study describes a simple method for testing the development of tolerance and its reversal with flumazenil or ZK 93426. At 72 h of pump infusion with diazepam or flunitrazepam, tolerance to anticonvulsant activity was evident. Acute treatment with flumazenil or ZK 93426 reversed this tolerance. When flumazenil or ZK 93426 was given to diazepam tolerant mice, this reversal was complete. In flunitrazepam tolerant mice reversal with flumazenil was partial, but significant. When flumazenil was chronically coinfused with diazepam or flunitrazepam, anticonvulsant activity was antagonized. Similarly, when ZK 93426 was coinfused with diazepam, anticonvulsant activity was antagonized. The method described is suitable for screening putative anticonvulsant drugs for development of tolerance and the reversal of tolerance by other compounds.

Animals↗
PubMed2006

Tolerance of shift work.

This study aimed to explore criteria for shift work tolerance and to investigate the relationships between personality traits and states and shift work tolerance. Eighty-nine policemen and police women completed a questionnaire, once during consecutive night shifts and again during rotating shifts, and their responses were used to assess anxiety, emotional control, positive and negative affect, health complaints, sleep quality, difficulties in social and domestic life, and perceptions about shift work. Both the criteria for tolerance and the relationship between tolerance and personality varied according to shift type. Night shift tolerance involved four factors--somatic health, flexibility, sleep and sleep need--while rotating shift tolerance involved three factors--somatic health, flexibility and fatigue. Tolerance of shift work was associated with anxiety, repressive emotional style and mood. During night shifts, anxiety was the most influential personality factor for the somatic health and sleep dimensions of shift tolerance. During rotating shifts, positive and negative moods, rather than trait personality factors, were important predictors of the somatic health and fatigue shift tolerance dimensions. These results suggest a mechanism for more effective matching of workers to suitable shift schedules.

Adult↗