Associations or repetitions? Testing the basis of the Perruchet effect in voluntary response speed.

The Perruchet effect refers to a dissociation between the conscious expectancy of an outcome and the strength or speed of responding in anticipation of that outcome. This dissociation is considered by some to be the best evidence for multiple learning processes with expectancy governed by participants' explicit beliefs and responding driven by the associative history of the cues that partially predict the outcome. However, an alternative nonassociative explanation is that the trends in responding are the result of recent experience with the same outcome (i.e., repetition priming based on event recency). This explanation casts doubt on the theoretical import of the dissociation because it suggests that associative learning may not be involved in generating the observed trends in response strength. Associative accounts of the Perruchet effect predict a weakening of the response strength trends when the cues perfectly predict the occurrence of the outcome. In two experiments, we compared a condition with two cues that were each perfect predictors of an outcome with control conditions in which the cues did not perfectly predict the outcome. In both experiments, the typical downward trend in response time (RT) observed in Perruchet effect experiments was substantially weaker (and indeed absent) for the predictive group, suggesting an associative contribution to the effect. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Testing the limits of the Perruchet effect in choice response time tasks.

The Perruchet effect refers to a dissociation between trends in the conscious expectancy of an event and trends in the strength or the speed of responding to that event, which suggests that learned changes in the performance of a response may be automatic. Despite being consistently demonstrated in conditioning studies and simple reaction time (RT) tasks, mixed results have been found in the choice variant of the Perruchet effect, especially when expectancy and responding are measured concurrently (that is, on the same trial). The present experiments examined why the dissociation disappears when concurrent measurement is used by directly comparing trials on which expectancy is measured to trials on which expectancy is not measured. In Experiment 1, expectancy was measured on a randomly chosen 50% of trials, whereas expectancy was measured every fourth trial in Experiment 2. In both experiments, the Perruchet effect was weakened on trials that immediately followed an expectancy rating but was still clearly evident on other trials, suggesting that automatic facilitation of RT based on recent trial history is temporarily masked, rather than abolished, by a concurrent expectancy judgment. (PsycINFO Database Record

The 6-min walk and peak oxygen consumption in advanced heart failure: aerobic capacity and survival.

BACKGROUND: This study sought to determine to what extent the 6-min walk (6MW) distance in advanced heart failure predicts aerobic capacity and provides comparable information regarding survival. Peak oxygen uptake ( VO(2)) and the 6MW both describe function and predict outcome over a wide range of heart failure, but their determinants and implications may differ within a narrower clinical spectrum. This study compared 6MW with aerobic capacity both at peak exercise and during low-level cycling. METHODS AND RESULTS: Both the 6MW and symptom-limited cycle ergometry were performed by 307 patients of whom 264 patients additionally performed 6 min of 20-W cycling to estimate aerobic capacity during sustained low-level activity. In the first 198 patients, multivariate analysis of survival was performed with the 6MW and peak VO (2). Patients achieved the 6MW of 393 +/- 104 m and peak VO (2) of 14 +/- 5 mL/kg per minute. Although low peak VO (2) was more likely with the shorter 6MW, the relation was weak within peak VO (2) range of 10 to 20 mL/kg per minute (n = 213, 69% of patients, r = 0.28). During 20-W exercise, VO (2) was 9.2 +/- 2.0 mL/kg per minute, with respiratory exchange ratio poorly correlated with the 6MW. In contrast to peak VO (2), the 6MW in meters did not predict survival. Division into short, medium, and long walks, however, supplemented simple clinical description. CONCLUSIONS: Although helpful in broader populations for identification of patients with obvious clinical compromise, the 6MW distance is not a surrogate for peak VO (2) in assessing aerobic capacity or prognosis for individuals with advanced heart failure.

Excessive oxygen deficit during low-level exercise in heart failure.

Although peak oxygen consumption is reduced in patients with symptomatic heart failure, the degree of limitation during routine activity often appears greater or lesser than expected from peak capacity. This study was undertaken to determine whether abnormalities could be detected during the initiation of steady-state low-level exercise, approximating routine activity, which were distinct from limitation in peak capacity. We sought to determine whether a delay in the integrated response to the increased metabolic demand caused by exercise, assessed by the oxygen deficit incurred between exercise initiation and the achievement of steady-state oxygen uptake, was present in heart failure. Low-level and symptom-limited maximal exercise tests in 33 ambulatory patients with heart failure were analyzed and compared with 9 tests in control subjects. Oxygen deficit was determined during the 8-minute low-level exercise at 20 W. During maximal exercise, as expected, patients with heart failure had lower peak oxygen uptake (16 +/- 4 vs 31 +/- 6 ml/kg/min) and anaerobic threshold (870 +/- 270 vs 1,180 +/- 370 ml/min) than controls. After 8 minutes of low-level exercise, the oxygen deficit was higher in patients than in controls (550 +/- 230 vs 270 +/- 100 ml, respectively, p < 0.01). Among patients with heart failure, the oxygen deficit did not correlate with peak oxygen uptake or anaerobic threshold. Although the time to steady-state heart rate was later in patients with heart failure, this delay did not correlate with oxygen deficit. The oxygen deficit represents a distinct abnormality of exercise response that may reflect impaired central and peripheral responses to the initiation of exercise.

Prognostic usefulness of positive or negative exercise stress echocardiography for predicting coronary events in ensuing twelve months.

Stress echocardiography is useful in diagnosing myocardial ischemia in patients with significant coronary artery disease. This study examines the correlation between the results of exercise stress echocardiography and cardiac event rates within 12 months after testing in patients referred for evaluation of possible myocardial ischemia. Cardiac events, defined as myocardial infarction, coronary artery bypass surgery, percutaneous transluminal coronary angioplasty or death, were tabulated for 360 patients with > or = 12 months of follow-up, or a cardiac event within 12 months of follow-up, or both. Wall motion abnormalities at rest were present in 60% of patients. A positive stress echocardiogram, defined as the development of new or worsened wall motion abnormalities, was obtained in 18% of patients (65 of 360), and > or = 1 cardiac event during follow-up was present in 14% (n = 49). A cardiac event occurred in 34% of patients (22 of 65) with a positive stress echocardiogram and in 9% (27 of 295) with a negative one. Myocardial infarctions occurred in 9% of patients with a positive stress echocardiogram compared with 2% with a negative test. An insufficient exercise capacity to reliably exclude ischemia was present in 63% of patients (17 of 27) with a cardiac event despite a negative stress echocardiogram. The predictive value of the stress echocardiographic results was enhanced by combining these results with the electrocardiographic results. In summary, a positive stress echocardiogram was associated with a threefold increased incidence of any cardiac event, and a fourfold increased incidence of myocardial infarction within 12 months of follow-up compared with a negative stress echocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise capacity for survivors of cardiac transplantation or sustained medical therapy for stable heart failure.

Cardiac transplantation is predicted to improve survival for patients with severe symptoms of heart failure and ejection fraction of 20% or less, but the exercise capacity after cardiac transplantation is less than normal. Patients responding to vasodilators and diuretics have progressive improvement in exercise capacity despite low ejection fraction. We hypothesized that among patients currently considered appropriate for transplantation who could nonetheless subsequently be stabilized on medical therapy tailored to hemodynamic goals, survivors after 6 months of sustained medical therapy would demonstrate exercise capacity comparable to that of survivors of transplantation. Of 146 patients referred, 118 (81%) were discharged on tailored therapy without transplantation, and 88 (60%) were stable for at least 1 month. Stability after discharge was more likely in patients with lower right atrial pressures and better renal function on therapy. Of the 88 stable patients, 45 patients were listed for transplant, and 43 were ineligible or unwilling. From these patients, 42 survivors for more than 6 months follow-up after cardiac transplantation or tailoring of medical therapy underwent exercise testing. Baseline functional and hemodynamic status and left ventricular ejection fraction (15 +/- 4%) were not different between the transplant and sustained medical survivor groups at the time of initial evaluation. After 14 +/- 6 months, left ventricular ejection fraction had increased to 62 +/- 7% after transplantation (p less than 0.01) and only 22 +/- 9% after sustained medical therapy (p less than 0.05). However, there were no significant differences in the maximum workload, oxygen uptake, anaerobic threshold, or maximum oxygen pulse between survivors of cardiac transplantation and survivors on sustained medical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Tumor killing by human alveolar macrophages and blood monocytes. Decreased cytotoxicity of human alveolar macrophages.

Tumor killing by human alveolar macrophages (AM) might be an important mechanism of pulmonary defense against neoplastic disease. We compared AM and blood monocytes (Mo) for the ability to kill 2 neoplastic targets, A549 human lung adenocarcinoma cells and P815 mastocytoma cells. Blood monocytes were able to kill both targets, whereas AM killed neither. Tumor killing by Mo was spontaneous and was not increased by incubation with lipopolysaccharide. Because the P815 target is highly sensitive to lysis by hydrogen peroxide (H2O2), it afforded the opportunity to compare AM and Mo for the ability to kill tumors by the production of toxic oxygen compounds. Comparable amounts of superoxide anion were produced by AM and Mo after stimulation with phorbol myristate acetate. However, luminol-enhanced chemiluminescence of AM was far less than that of Mo, suggesting that AM could not utilize the myeloperoxidase-H2O2-halide ion system for tumor killing. The addition of exogenous peroxidase to cultures of AM and P815 cells enabled AM to kill this tumor cell. Our results suggest that as Mo mature into AM, their ability to kill tumor cells declines and that AM may be unable to kill H2O2-sensitive tumors because of a loss of myeloperoxidase during maturation.

Human alveolar macrophages: HLA-DR-positive macrophages that are poor stimulators of a primary mixed leukocyte reaction.

Previous studies demonstrated that alveolar macrophages (AM) from most normal human volunteers failed to stimulate the antigen-induced proliferation of peripheral blood T lymphocytes although greater than 90% of AM expressed HLA-DR antigens. The current studies establish that AM also fail to induce allogeneic peripheral blood mononuclear cells to proliferate in a mixed leukocyte reaction (MLR). Suppressive activity by AM was not an explanation for their failure to induce an MLR. Indirect immunofluorescence established the presence of both HLA-DR and DQ antigens on the majority of AM and the persistence of these antigens on cells in culture for up to 6 days, the period of time required to observe a maximal MLR. Metabolic labeling experiments also demonstrated that HLA-DR antigens were synthesized by AM. It was recently reported that AM secrete relatively small amounts of IL 1, an important ancillary signal provided by accessory cells to enhance the stimulation of lymphocyte proliferation. However, addition of optimal concentrations of IL 1 to cultures containing AM failed to enhance the MLR. Thus, there is at least one additional, but as yet undefined, requirement for an accessory cell to induce an optimal MLR besides the display of HLA-D region antigens and the secretion of IL 1. In contrast, AM were effective in specifically stimulating proliferation of alloreactive T cell lines, suggesting that at least some cell lines do not require this nonspecific undefined second signal. We speculate that although AM may not initiate primary immune responses in the lung, they may be important in maintaining immune-mediated inflammatory responses by specifically restimulating already activated T cells.

Bronchoalveolar cells from sarcoid patients demonstrate enhanced antigen presentation.

The recognition of foreign antigens by T lymphocytes in association with lung antigen-presenting cells may be critical in the initiation of the mononuclear alveolitis and granuloma formation of pulmonary sarcoidosis. However, it has been shown that bronchoalveolar cells (BAC) from normal volunteers function poorly as antigen-presenting cells. Therefore, the ability of sarcoid BAC to serve as accessory cells for antigen-dependent autologous T cell proliferation, as measured by tritiated thymidine uptake, was compared with that of normal BAC. Although irradiated sarcoid BAC supported antigen-induced T cell proliferation, normal BAC did so poorly (p less than 0.005). Because it has been shown that sarcoid BAC produce more interleukin 1 (IL 1) than normal BAC, it was considered that the enhancement of antigen-induced proliferative responses could result from an increased amount of IL 1, and that contaminating monocytes in the peripheral blood T cell preparations displayed the antigen for T cell recognition. Therefore, it was necessary to establish that antigen-induced T cell responses required HLA-D region compatibility between the sarcoid BAC and T lymphocytes. BAC from sarcoid patients stimulated antigen-specific proliferation in T cells lines matched for at least one HLA-D-region antigen, but failed to stimulate T cell lines that were unmatched for both antigens. This finding indicates that cells in bronchoalveolar lavage fluids from sarcoid patients were fully capable of acting as antigen-presenting cells. The identification of antigen-presenting cells in the lungs of patients with sarcoidosis together with the previous findings of activated T cells, enhanced IL 1 production, and spontaneous interleukin 2 release in sarcoid patients is compatible with the hypothesis that local cell-mediated immunity is involved in the pathogenesis of pulmonary sarcoidosis.